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PLATE  I 


NERVOUS  DISEASES 

DANA 


The  Fiest  Formal  Union  of  Neuro- anatomy  and  Art.     {Ste-phmius,  1545.) 

"  The  avulsed  calvarium  hangs  from  a  tree,  showing  the  dura  mater." 


TEXT-BOOK 

OF 


NERVOUS  DISEASES 


FOR  THE  USE  OF  STUDENTS  AND 
PRACTITIONERS  OF  MEDICINE 


BY 
CHARLES  L.  DANA,  A.  M.,  M.  D.,  LL.  D. 

PROFESSOR    or    NERVOUS   DISEASES   IN    CORNELL   UNIVERSITY  MEDICAL  COLLEGE;  CONSULTING  PHYSICIAN 
TO  BELLEVUE   HOSPITAL;      NEUROLOGIST     TO   THE     MONTEPIORE     HOSPITAL;    NEUROLOGIST     TO 
THE     woman's     hospital;      consulting      PHYSICIAN     TO     THE     MANHATTAN     STATE 
hospital;      EX-PRESIDENT    OP     THE     AMERICAN   NEUROLOGICAL    ASSOCIATION; 
EX-PRESIDENT   OP   THE    NEW    YORK     ACADEMY     OP     MEDICINE;     CORRE- 
SPONDING    MEMBER     or     THE     SOCIETE   DE   NEUROLOGIE,    ETC. 


EIGHTH   EDITION 


WITH  TWO  HUNDRED  AND  SIXTY-TWO  ILLUSTRATIONS, 
INCLUDING  FOUR  PLATES  IN  BLACK  AND  COLOR 

\ 


NEW  YORK 

WILLIAM  WOOD  AND  COMPANY 

MDCCCCXV 


Copyright,  1915,  by 
WILLIAM  WOOD  AND  COMPANY 


XHE    MAPIiE     PKESS    YOKK    FA 


PREFACE  TO  THE  EIGHTH  EDITION 

When  the  first  edition  of  my  book  was  published  twenty-three  years 
ago  there  was  no  adequate  description  of  the  anatomy  of  the  nervous 
system  in  the  English  language.  Hence,  feeling  the  fundamental  im- 
portance of  this  subject  to  an  understanding  of  neurology,  I  gave  much 
space  to  it.  This  need  of  anatomical  knowledge  of  the  nervous  system 
is  now  abundantly  supplied  by  general  and  special  text-books.  I  have, 
therefore,  left  out  a  good  deal  of  this  part  of  my  text.  I  have  retained 
and  revised  what  was  especially  useful  in  diagnosis  and  for  reference, 
and  have  also  changed,  added  to  and  improved  the  illustrations.  In 
this  I  have  received  help  and  skilled  supervision  from  Dr.  J.  F.  Guder- 
natsch,  of  the  Anatomical  Department  of  Cornell  University. 

A  large  part  of  the  rest  of  the  book  has  been  completely  remodeled 
and  rewritten.  This  applies  to  the  chapters  on  syphilis  of  the  nervous 
system,  including  paresis,  tabes  and  the  serology  of  nervous  diseases. 
Dr.  David  Kaplan,  of  the  New  York  Neurological  Institute,  has  furnished 
me  with  data  on  this  last  subject  which  represent  large  experience  and 
bring  the  matter  to  date. 

The  chapter  on  acute  anterior  poliomyelitis  has  been  rewritten  by 
Dr.  Foster  Kennedy  in  the  light  of  recent  discoveries,  and  the  same  has 
been  done  for  the  chapter  on  epidemic  cerebrospinal  meningitis  by  Dr. 
H.  W.  Frink.  I  am  under  obligations  to  both  these  gentlemen  for  their 
excellent  work. 

Practically  new  chapters  have  been  written  on  tumors  of  the  spinal 
cord  and  tumors  of  the  brain.  Dr.  Charles  A.  Elsberg  has  allowed  me 
to  use  the  statistics  of  his  cases,  so  that  I  am  able  to  present  these  topics 
from  the  standpoint  of  modern  neurological  surgery  as  well  as  of  medicine. 

The  chapters  on  methods  of  examination  and  diagnosis  and  on  general 
symptoms  have  been  thoroughly  revised  and  an  endeavor  made  to  include 
the  latest  data.  The  number  of  epinomic  signs  and  syndromes  of  neurol- 
ogy has  grown  to  a  burdensome  length.  A  descriptive  list  of  them  has 
been  prepared  by  Dr.  Frink. 

The  chapters  on  the  psycho-neuroses  have  been  rearranged  and  in 
parts  rewritten  and  condensed.  Neurasthenia  has  been  pushed,  as 
modern  views  demand,  much  more  into  the  background.  Hysteria  and 
psychasthenia  have  been  treated  from  the  standpoint  of  descriptive  rather 
than  of  " dynamic"  or  analytic  neurology.  This  it  seemed  to  me  was  the 
only  way  to  make  the  subject  intelligible  in  a  work  meant  largely  for 

iii 


IV  PREFACE  TO  THE  EIGHTH  EDITION 

students  and  practitioners.  I  trust  that  I  have,  however,  given  a  measure 
of  justice  to  psycho-analysis,  as  it  certainly  has  a  place  in  the  interpreta- 
tion and  occasionally  in  the  therapeutics  of  the  minor  psychoses. 

The  subject  of  the  disturbances  of  growth  and  metabolism  and  of 
nervous  function  due  to  glandular  disorders  has  brought  out  a  large 
literature  in  recent  years,  and  this  has  been  considered  in  the  revision  of 
this  edition. 

The  subject  of  therapeutics  is  difficult  to  discuss  effectively  in  a  trea- 
tise that  aims  to  be  of  moderate  size.  Methods  and  drugs  and  points  of 
view  change  so  rapidly  that  I  have  decided  to  leave  out  the  special  chapter 
on  this  subject.  Treatises  on  electricity,  massage,  exercise,  diet,  mechan- 
ical therapy,  hydrotherapy,  etc.,  are  now  many  and  accessible. 

Many  new  clinical  and  anatomical  illustrations  have  been  added. 
I  am  greatly  indebted  to  Dr.  J.  B.  Gere,  of  the  Pathological  Department 
of  Cornell  University  Medical  College,  for  beautiful  photographs  of 
spinal-cord  and  of  nerve  disease; to  Dr.  S.  Wachsmann  and  the  Montefiore 
Home  for  photographs  of  clinical  cases;  and  to  Dr.  R.  S.  MacRobert,  of 
New  York  Neurological  Institute,  for  photographs  illustrating  methods 
of  examination.  A  modest  tribute  has  been  paid  to  the  fathers  of  neuro- 
anatomy in  the  reproduction  and  use  of  illustrations  of  the  brain  by 
Stephanus,  Willis,  and  Ruysch.  They  represent  anatomical  illustration 
and  art  in  the  16th,  17th  and  18th  centuries  respectively. 

The  part  of  my  work  devoted  to  psychiatry  will  appear  in  a  separate 
volume.  However,  I  have  included  in  the  present  treatise  articles  on 
the  minor  psychoses,  as  well  as  a  chapter  on  paresis. 

A  treatise  on  neurology  must  usually  be  read,  and  studied  in  parts, 
hence  that  portion  of  the  original  preface  has  been  retained  which  sug- 
gested to  the  reader  a  certain  eclecticism  of  method  in  neurological 
study.  The  principle  then  set  forth  holds  good  now  though  the  lists 
then  given  need  revision. 

My  thanks  are  due  to  my  publishers  for  their  helpfulness  and  cheerful 
co-operation. 

New  York  City, 

Sept.,   15,    1915. 


FROM  PREFACE  TO  THE  FIRST  EDITION 


As  a  special  text-book  the  present  work  will  be  used  by  two  classes 
of  readers,  one  consisting  of  those  who  simply  consult  it  for  reference  in 
connection  with  their  cases,  the  other  composed  of  students  who  desire 
to  ground  themselves  systematically  in  a  knowledge  of  neurology.  To 
this  latter  class  I  venture  some  advice  as  to  the  method  they  should  pur- 
sue. Neurology  is  a  difficult  branch  of  medicine  to  master,  nor  is  there 
any  royal  road  to  it.  Still,  it  can  be  made  comparatively  easy  if  its 
study  is  undertaken  in  a  proper  and  systematic  way. 

In  using  the  present  work,  the  student  should  first  refresh  his  general 
knowledge  of  nervous  anatomy  as  furnished  in  ordinary  text-books.  He 
should  then  go  carefully  over  the  anatomical  descriptions  here  given  of 
the  general  structure  of  the  nervous  system  and  of  that  of  the  nerves, 
spinal  cord,  and  brain.  A  thorough  knowledge  of  anatomy  and  physiol- 
ogy makes  clinical  neurology  comparatively  easy,  and  in  fact  reduces 
much  of  it  simply  to  a  matter  of  logical  deduction. 

The  student  should  next  master  the  general  facts  of  nervous  path- 
ology, symptomatology,  and  etiology,  for  he  will  find  common  laws 
underlying  apparently  the  most  varying  phenomena.  Finally,  he  must 
begin  to  study  the  special  diseases.  The  number  of  these  is  very  great; 
in  the  present  work  I  have  described  176.  Many  of  these  are  rare,  and 
it  would  be  wrong  for  the  student  to  burden  his  memory  with  the  details 
about  them.  He  need  know  only  of  their  existence  and  general  physiog- 
nomy. There  are,  however,  according  to  my  enumeration,  about  65 
nervous  diseases  which  are  either  very  common  or  extremely  important, 
and  it  is  these  that  the  student  should  master  and  make  part  of  his  work- 
ing knowledge.  Since  the  distribution  and  names  of  the  common  and 
rare  diseases  may  be  a  useful  guide,  I  append  here  a  table  and  a  list : 


Peripheral 

Spinal 
Cord 

Brain 

Functional 

Totals 

Common  and  important  dis- 
eases   

Pi,are 

31 
56 

13 

27 

12 
16 

10 
11 

66 
110 

87 

40 

28 

21 

176 

The  common  or  important  nervous  diseases  are: 
General. — Neuritis,  multiple  neuritis,   degeneration,   neuralgia,   par- 
sesthesia  (5). 


VI  PREFACE 

Cranial  Nerves. — Anosmia,  optic  neuritis,  optic  atrophy,  ptosis, 
ophthalmoplegia,  abducens  palsy,  headache,  migraine,  trigeminal  neural- 
gia, facial  spasm,  facial  palsy,  tinnitus,  vertigo,  ageusia,  wryneck  (16). 

Spinal  Nerves. — Cervical  neuralgia,  hiccough,  brachial  palsies,  single 
and  combined,  brachial  neuralgia,  intercostal  neuralgia,  herpes  zoster, 
lumbar  neuralgia,  sciatica,  leg  palsies  (10). 

Spinal  Cord. — Spina  bifida,  hemorrhage,  pachymeningitis,  lepto- 
meningitis, poliomyelitis,  transverse  myelitis,  acute  and  chronic,  second- 
ary degenerations,  locomotor  ataxia,  the  progressive  muscular  atrophies, 
bulbar  palsy,  muscular  dystrophies,  spinal  irritation  (13). 
,  Brain. — Malformations,  hypersemia,  pachymeningitis,  leptomenin- 
gitis, simple,  tuberculous,  and  epidemic,  abscess,  hemorrhage,  embolism, 
thrombosis,  children's  palsies,  syphilis  (12). 

Functional.- — -Epilepsy,    hysteria,  the  tics,   chorea,  tetanus,   neuras- 
thenia, spermatorrhoea,  exophthalmic  goitre,   occupation  neuroses,  pa- 
ralysis agitans  (10). 
New  York  City,  1892. 


TABLE  OF  CONTENTS 

CHAPTER  I 

Page 
General  Anatomy,  Physiology,  and  Chemistry.     The  General  Histology  of 

the  Nervous  System — The  Neuronic  Architecture  of  the  Nervous  SJ^stem   .    .        1 

CHAPTER  II 

The  Causes  of  Nervous  Diseases      23 

CHAPTER  III 
General  Pathology 28 

CHAPTER  IV 

General  Symptoms    30 

CHAPTER  V 

Diagnosis  and  Methods  of  Examination.  Examination  of  the  Reflexes — 
Examination  of  the  Disorders  of  Sensation — Cerebrospinal  Fluid — Spinal 
Puncture 39 

CHAPTER  VI 

Hygiene,  Prophylaxis,  Treatment.  Diet — Exercise — Hj^drotherapy — 
Massage — Osteopathy — Climate — Electricity — Radiant  Energy — Psycho- 
therapy   60 

CHAPTER  VII 

Diseases  of  the  Peripheral  Nerves.  General  Pathology — Hypersemia  and 
Anaemia — Angina — Neuritis — Degeneration — General  Symptoms — Multiple 
Neuritis — Sensory-motor  Type — Sensori-ataxic  Type — Endemic  and  Epi- 
demic Types — Malarial — Acute  Pernicious — Complicating  Forms  of 
Neuritis  and  Neuritic  Degeneration — Tumors 75 

CHAPTER  VIII 

Motor  Disorders  of  Cranial  Nerves.  The  Ocular  Muscles — General  Symp- 
toms— The  Ophthalmoplegias — Third  Nerve — Fourth  Nerve — Sixth  Nerve 
— Muscular  Asthenopia  and  Muscular  Insufficiencies — Spasmodic  Diseases 

vii 


VIU  CONTENTS 

Page 
of  the  Ocular  Muscles — The  Motor  Branch  of  the  Fifth  Cranial  Nerve — The 
Facial  Nerve — Facial  Spasm — Facial  Palsies — The  Glossopharyngeal  Nerve 
— The  Pneumogastric  Nerve  and  the  Accessory  part  of  the  Spinal  Accessory 
— Vagotonia — Laryngeal  Nerve  Supply — Spinal  Part  of  the  Accessorius  and 
Upper  Cervical  Nerves — Torticollis — Paralysis  of  the  Spinal  Accessory — The 
Hypoglossus — The  Mechanism  of  Articulation 95 

CHAPTER  IX 

Neuroses  of  the  Motor  Spinal  Nerves.  The  Upper  Cervical — The  Lower 
Cervical  and  Brachial  Plexus — The  Thoracic  or  Dorsal — The  Lumbar 
—The  Sacral 126 

CHAPTER  X 

Sensory  Neuroses  of  the  Cerebrospinal  Nerves.  Parsesthesia — Neuralgia — 
Neuroses  of  the  Nerves  of  Special  Sense — The  Olfactory  Nerve — The  Optic 
Nerve — Trigeminal  Nerve — Headache — Migraine — Seventh  Nerve — Acous- 
tic Nerve — Nervous  Deafness — -Tinnitus  Aurium — Vertigo — Glossopharyn- 
geal Nerve — Upper  Cervical  Nerves — ^Lower  Cervical  Nerves  and  Brachial 
Plexus — Intercostal  Nerves — Lumbar  Nerves — Peripheral  Vasomotor  and 
Trophic  Neuroses 145 

CHAPTER  XI 

Diseases  of  the  Spinal  Cord.  Anatomy  and  Physiology — Diagnostic  Physi- 
ology   200 

CHAPTER  XII 

Diseases  of  the  Spinal  Cord.  Malformations — Spina  Bifida — Spinal  Hemor- 
rhage— The  Caisson  Disease — Spinal  Meningitis — Myelitis  and  Myelo- 
malacia— Poliomyelitis — Acute   Ascending   Paralysis 214 

CHAPTER  XIII 

Scleroses,  Degenerations,  Syphilis.  Locomotor  Ataxia — Lateral  Sclerosis — 
The  Combined  Scleroses — Hereditary  Spinal  Ataxia — Hereditary  Cere- 
bellar Ataxia 248 

CHAPTER  XIV 

The  Progressts^e  Muscular  Atrophies  and  Muscular  Dystrophies.  Luetic 
Spinal  Atrophy — Hereditary  Muscular  Atrophy  of  the  Peroneal  Tj'pe — 
Glosso-labio-larjrngeal  Paralysis  —  Myasthenia  Gravis  —  Amyotrophic 
Lateral  Sclerosis — The  Progressive  Muscular  Dystrophies — Pseudo- 
muscular  Hypertrophj^ — Hemihypertrophy — Summary  of  the  Hereditary 
or  Family  Nervous  Diseases — Arthritic  Muscular  Atrophy — Occupation 
Muscular  Atrophies 292 


CONTENTS  IX 

CHAPTER  XV 

Page 

Tumors    and    Cavities    of    the    Spinal    Cord.     Hydromyelia — Gliosis    and 

Syringomyelia — The  Recognition  of  Diseases  of  the  Cauda  Equina    ....   318 

CHAPTER  XVI 

Anatomy  and  Physiology  of  the  Brain.     The  Cerebellum — The  Glands  of  the 

Brain — The  Connecting  Tracts — The  Membranes — The  Functions ....   333 

CHAPTER  XVII 

Diseases  of  the  Brain  and  Its  Membranes.  General  Symptoms — Malforma- 
tions— Purulent  Cerebrospinal  Meningitis — Epidemic  Cerebrospinal  Menin- 
gitis— Tuberculous  Meningitis — Hydrocephalus — Alcoholic  Meningitis — 
Hypersemia   and    Anaemia 367 

CHAPTER  XVIII 

Diseases  of  the  Brain.  Inflammations— General  Paresis — Multiple  Sclerosis 
— The  Apoplexies — Softening — Sinus-thrombosis — Cerebral  Palsies  of 
Children 395 

CHAPTER  XIX 

Tumors  of  the  Brain.     Intracranial  Aneurism      454 

CHAPTER  XX 

Functional  and  Degeneratr^e  Diseases.     Epilepsy 474 

CHAPTER  XXI 

The  Psycho-neuroses.     Constitutional  Inferiority — Hysteria      488 


CHAPTER  XXII 
Psychasthenia 507 

CHAPTER  XXIII 

Neurasthenia.     The    Sexual    Neuroses    and    Psychoses — Traumatic    Nervous 

Affections 514 

CHAPTER  XXIV 

The  Myoclonias  or  Twitching  Spasms.  Chorea  of  Sydenham — Hereditary 
Chorea — Spasmodic  Tic — Fibrillary  Myoclonia — -Myotonia — Tortipelvis — 
Tetanus — Tetany — Rabies  and  Hydrophobia 535 


X  CONTENTS 

CHAPTER  XXV 

Page 
Exophthalmic  Goitre  and  Hyperthyroidism v.   553 

CHAPTER  XXVI 

Professional  Neuroses,  Occupation  Neuroses      560 

CHAPTER  XXVII 
Paralysis  Agitans 667 

CHAPTER  XXVIII 

Trophic  and  Vasomotor  Disorders.     Hemiatrophy — Diseases  of  the  Pituitary 

Gland — Acromegaly — Myxoedema — Cretinism — Angio-neurotic  CEdema  .    .    576 

CHAPTER  XXIX 

The  Disorders  op  Sleep.  Insomnia — Hypnotism — Morbid  Somnolence — 
Catalepsy — Trance — Lethargy — Perversions  and  Disturbances — Mesmer- 
ism— The  Sleeping  Sickness  of  Africa 586 

CHAPTER  XXX 
Cranio-cerebral  Topography 600 

APPENDIX 

The  Function  and  Innervation  of  the  Muscles.  Muscles  of  Tongue,  Palate 
and  Pharynx — Muscles  of  Head  and  Neck — Muscles  of  Shoulder  and  Upper 
Extremity — Muscles  of  Arm,  Forearm  and  Hand — Muscles  of  Back  and 
Lower  Extremities 605 


PAET  I 
DISEASES  OF  THE  NERVOUS  SYSTEM 


CHAPTER  I 
GENERAL  ANATOMY,  PHYSIOLOGY,  AND  CHEMISTRY 

In  studying  the  phenomena  of  hfe  in  tlie  human  body,  we  as  physicians 
first  learn  about  its  normal  structure  and  functions.  We  then  note  the 
new  phenomena  which  develop  when  disease  comes  on,  the  causes  which 
produce  them,  and  the  anatomical  changes  lying  back  of  them;  we  group 
our  facts  and  give  the  disease  a  name.  Lastly  we  apply  the  methods 
by  which  the  disorder  can  be  expelled  and  future  attacks  prevented.  In 
fine,  we  investigate  our  subject  just  as  we  do  that  of  any  branch  of  natural 
history.     Our  study  divides  itself,  therefore,  into 

Normal  anatomy  and  physiology. 

Etiology,  a  study  of  the  causes. 

Symptomatology,  a  study  of  the  morbid  phenomena. 

Pathology,  under  which  we  include  a  study  of  the  morbid  anatomy 
and  physiology. 

Diagnosis,  or  the  method  of  recognizing  and  separating  out  the  dif- 
ferent groups  of  diseases. 

Prognosis,  a  forecast  of  the  future  course  of  the  malady. 

Treatment  and  prophylaxis. 

GENERAL  ANATOMY 

The  nervous  system  is  derived  from  the  ectodermal  germ  layer  of 
the  developing  ovum,  and  its  constituents  are  modifications  of  epithelial 
cells.  These  cells  in  the  embryo  are  of  two  kinds:  neuroblasts,  which 
develop  into  nerve-cells  and  fibres;  and  spongioblasts,  which  develop 
into  a  supporting  structure  called  neuroglia  (His). 

The  nervous  system  is  composed  of: 

(a)  Neurons,  which  form  the  nervous  tissue  proper,  and  are  made  up 
of  nerve-cells,  with  their  processes,  one  of  which  becomes  an  axis  cylinder; 
and  neuroglia. 

(6)  Accessory  tissue,  consisting  of  connective  tissue,  blood-vessels, 
lymphatics,  and  epithelium. 


DISEASES    OF    THE    NERVOUS    SYSTEM 


These  tissues  are  united  together  to  form  the  central  nervous  system, 
consisting  of  the  brain  and  spinal  cord,  and  the  peripheral  nervous 
system.  This  latter  is  composed  of  nerve-fibres,  and  structures  attached 
to  the  terminations  of  the  nerves,  called  end-organs,  and  finally  the 
ganglionic  or  sympathetic  nervous  system  is  included  in  the  peripheral 
system. 

The  Arrangement  of  the  Nervous  System. — The  subdivisions  of  these 
parts,  and  their  descriptions  in  detail,  belong  to  general  anatomy. 
But  there  have  been  so  many  special  subdivisions,  and  particular  names 
given  to  them  in  recent  years,  that  I  deem  it  necessary,  in  order  to  pre- 
vent confusion,  to  describe  briefly  the  subdivision  accepted  by  modern 
anatomists.  The  names  here  used  are  those  adopted  by  the  committee  on 
anatomical  nomenclature  of  the  German  Anatomical  Society,  and  they 
have  also  been  adopted  by  a  large  number  of  writers  on  neuro-anatomy. 


vAjO^/j, 


''""MAL/c 


OPTIC  VESICLE 


Fig.  1. 


-Showing  divisions  of  embryonal  human  brain  in  third  and  fifth  weeks. 
(His.)  (Cunningham.) 


Beginning  with  the  brain,  we  find  that  its  particular  subdivisions  are 
based  upon  the  embryological  development  of  this  organ.  As  will  be 
shown  in  more  detail  later,  the  brain  is  developed  out  of  three  vesicles, 
known  as  the  anterior,  middle,  and  posterior  vesicles  (Fig.  1).  The  most 
anterior  of  these  vesicles  is  the  prosencephalon  or  anterior  brain;  the  middle 
vesicle  becomes  the  mesencephalon  or  mid-brain,  and  the  posterior  vesi- 
cle develops  into  the  rhombencephalon  or  posterior  brain. 

The  anterior  vesicle  develops  two  secondary  vesicles :  the  anterior  por- 
tion of  these,  including  the  corpora  striata,  olfactory  lobes  and  the  cere- 
bral hemispheres,  forms  the  telencephalon  (Fig.  2, 1 2),  while  the  hinder  por- 
tion of  this  vesicle,  which  includes  the  thalamus  and  mammary  bodies, 
forms  the  diencephalon  (I^).  The  middle  vesicle  is  the  mesencephalon, 
and  it  includes  the  corpora  quadrigemina  and  cerebral  peduncles  (II). 


GENERAL    ANATOMY,    PHYSIOLOGY,    AND    CHEMISTRY 


3 


The  posterior  vesicle  is  divided,  from  before  backward,  into  three  different 
parts:  (1)  the  isthmus,  which  inchides  the  superior  cerebellar  peduncles 
and  valve  of  Vieussens,  and  part  of  the  cerebral  peduncles;  (2)  the 
metencephalon  or  hind-brain,  which  includes  the  cerebrum  and  pons 
Varolii;  and  (3)  the  myelencephalon  or  after-brain,  which  includes  the 
medulla  oblongata. 


Prosencephalon 
(anterior  brain). 
II  and  1= 


Brain.    <!  Mesencephalon 

(middle  brain).  H 

Rhombencephalon 
(posterior  brain). 
Ill  and  IV 


1.  Telencephalon. 

2.  Diencephalon. 

[  3.  Mesencephalon. 

4.  Isthmus. 

5.  Metencephalon. 

6.  Myelencephalon. 


Hemispheres. 

Pars  optica  hypothalami. 

Pars  mammalians. 

Thalamus. 
/  Pedunculi  cerebri. 
\  Corpora  quadrigemina. 

Cerebellum. 
Pons. 
!  Medulla  oblongata. 


These  different  parts  can  be  understood  better  by  means  of  the 
accompanying  figure  (Fig.  2),  which  represents  in  a  schematic  way  the 
brain  of  a  mammal. 


Fig.  2. 


They  are  intimately  connected  by  strands  of  nerve-fibres,  and  are 
connected  closely  also  with  the  next  portion  of  the  nervous  system,  the 
spinal  cord.  The  brain  and  spinal  cord  are  spoken  of  as  the  cerebrospinal 
axis,  and  this  is  in  close  relation  with  the  peripheral  nervous  system. 

This  peripheral  nervous  system  is  composed  of  two  portions — -first, 
the  cerebrospinal  mixed  nerves,  whose  origin,  distribution,  and  relations 
are  comparatively  easy  to  follow;  and  second,  the  autonomic  or  sympa- 
thetic nervous  system.  This  portion  of  the  nervous  system  is  composed 
of  two  sets  of  ganglia — one,  the  vertebral  ganglia,  i.e.,  the  chain  of  gan- 
glionic masses  on  each  side  of  the  vertebral  column,  and  of  certain  ganglia 
connected  with  the  cranial  nerves;  secondly,  a  very  large  number  of 


4  DISEASES    OF    THE    NERVOUS    SYSTEM 

ganglionic  masses  distributed  in  the  viscera,  and  known  as  the  peripheral 
ganglia.  The  sympathetic  nervous  system  is  made  up  of  multipolar  cells 
and  of  some  medullated  (white),  but  mostly  of  non-medullated  (gray) 
naked  nerve-fibres. 

Efferent  white  fibres  pass  out  from  the  spinal  cord  through  the  anterior 
roots  and  pass  partly  to  the  sympathetic  ganglia  and  partly  continue  on  to 
the  viscera,  glands  and  blood-vessels.  Afferent  fibres  originate  in  the 
sympathetic  ganglia  and  pass  in  part  through  the  posterior  roots  to  the 
spinal  cord;  in  part  they  turn  and  pass  with  peripheral  nerves  to  the  skin, 
blood-vessels  and  glands. 


Fig.  3. — Nerve  cells  of  different  types,     a,  Unipolar;  h,  bipolar;  c,  pyramidal  cell; 
d,  Purkinje  cell.      (Villiger.) 


THE   GENERAL  HISTOLOGY  OF  THE  NERVOUS  SYSTEM 

The  nerve-cells  form  the  central  body  of  the  neuron  and  are  minute 
objects  varying  much  in  size.  Thelargest  are  0.1mm.  (>^5  0  in.)  in  diameter 
and  are  almost  visible  to  the  naked  eye.  The  smallest  are  0.7m  (K500  in.) 
in  diameter;  so  that  the  average  diameter  is  rather  greater  than  that  of  a 
white  blood-cell.  In  shape  nerve-cells  are  for  the  most  part  irregularly 
spheroidal,  but  some  are  pyramidal,  others  spindle-  or  flask-shaped,  and 
others  globular.  They  all  give  off  one  or  more  fine  processes  or  poles 
and  hence,  in  accordance  with  the  number  of  these,  the  nerve-cells  are 
often  spoken  of  as  multipolar,  bipolar,  or  unipolar. 

In  most  cells  one  of  the  processes  is  continued  on  a  long  way  and 
finally  becomes  a  nerve-fibre.     This  process  is  called  the  axis-cylinder,  or 


GENERAL    ANATOMY,    PHYSIOLOGY,    AND    CHEMISTRY  5 

neuraxon  or  axon  (Figs.  3,  4  and  5  and  Plate  II).  The  other  processes  are 
relatively  short  and  are  called  protoplasmic  processes,  or  dendrites.  The 
nerve-cell,  then,  is  a  protoplasmic  body  giving  off  several  dendrites  and 
usually  a  single  neuraxon,  the  whole  forming  the  neuron.  The  dendrites 
branch  off  irregularly  and  subdivide,  but  never  anastomose.  In  some  parts 
of  the  nervous  system  they  have  upon  them  little  nodules  or  buds,  and 
in  the  cerebral  and  cerebellar  cortex  these  are  so  numerous  as  to  give 


Fig.  4.  Fig.  5. 

Fig.  4. — -Nerve  cell  showing  dendrites,  axon,  collaterals,     a,  Axis-cjdinder-bifur- 
cating  at  h;  c,  a  collateral;  d,  varicosities  of  the  dendrites.     (Cajal.) 

Fig.  5. — Nerve  cells  from   anterior  horn  of  spinal   cord.      (Cunninghmn.) 

them  the  appearance  of  budded  stalks.  The  dendrites  are  usually  not 
very  long,  but  in  some  cells  they  extend  a  very  great  way,  reaching  many 
times  the  diameter  of  the  cell.  The  axis-cylinder  process,  or  neuraxon,  is 
given  off  directly  from  the  body  of  the  cell,  as  a  rule  (Fig.  5).  It  very  soon 
becomes  clothed  with  a  thin  sheath  (myelin  sheath) ,  and  as  it  passes  along 
gives  off  branches  at  right  angles,  which  form  what  are  known  as  the 
collaterals.     The  neuraxon  and  collaterals  finally  end  by  splitting  up  into  a 


6 


DISEASES    OF    THE    NERVOUS    SYSTEM 


number  of  fine  branches,  which  lose  their  myelin  sheath  and  form  the 
end-brush  or  terminal  arborization.  In  some  neurons  instead  of  an  end- 
brush,  there  are  several  minute  ovoid  bodies  which  lie  upon  the  cell  or  its 
dendrites.  They  are  called  "end-buds"  or  terminal  "buttons."  They 
are  seen  especially  in  the  medulla  and  pons,  but  not  in  the  cerebral  or 
cerebellar  cortex.  The  axis-cylinder  process  or  neuraxon  does  not  anas- 
tomose with  other  cells  either  through  its  own  end-brush  or  through  the 
end-brushes  of  its  collaterals.  The  end-brushes,  however,  pass  in  among 
the  dendrites  of  other  cells,  and  sometimes  closely  surround  the  cell-body. 
In  this  way  one  neuron  comes  into  very  intimate  relation  with  others,  but 
there  is  never  any  true  union.  Each  neuron  of  the  nervous  system  is  an 
independent  unit. 


Fig.  6. — Ganglionic  nerve  cells,  ultra-microscopical  illumination.     (Marinesco.) 


The  cell-body  proper  is  composed  of  a  cytoplasm.  Within  this  lies 
the  nucleus  and  within  the  nucleus  a  nucleolus.  The  body  proper  is 
not  homogeneous,  but  is  made  up  of  a  network  of  fine  fibres  or  fibrillse 
which  pass  in  bundles  from  dendrite  to  dendrite  and  from  dendrite  to 
the  neuraxon,  called  the  endocellular  fibrillar  network.  Within  its 
meshes  and  arranged  in  a  rather  definite  manner  are  certain  stainable 
bodies  called  Nissl  or  chromophilic  granules  (Plate  II).  The  chromo- 
philic  granules  are  arranged  differently  in  cells  of  different  function. 
They  are  believed  to  represent  the  functioning  substance  of  the  cell, 
while  the  fibrillse  form  a  conducting  part.  The  cell-body  usually  con- 
tains a  little  pigment. 


NERVOUS  DISEASES 
Dana 


PLATE  II 


B 


Nerve-cells  Stained  by  Nissl's  Method,  with  Toluidin  Blue.     Magnified 
675  diameters.    {Schaefer.) 

A,  From  anterior  horn  of  spinal  cord,  monkey;  B  and  C,  from  facial  nucleus,  dog;  D,  from  reticular 
formation  of  pons  Varolii,  dog;  C,  shows  Nissl  degeneration,  consequent  on  section  of  the  facial  nerve 
15  days  previously;  a, a,  axons. 


GENEKAL    ANATOMY,    PHYSIOLOGY,    AND    CHEMISTRY  7 

The  nucleus  of  the  cell  is  a  comparatively  large  spherical  body,  which 
is  also  made  up  of  a  reticulated  structure  known  as  the  chromatin  network. 
The  chromatin  consists  of  granules  resting  on  a  network  formed  by  the 
achromatic  substance  (hnin).  The  chromatin  is  practically  identical 
with  nuclein.  Within  the  nucleus  is  a  smaller  body,  known  as  the 
nucleolus,  which  stains  still  more  intensely. 

Nerve-cells  are  surrounded  by  a  pericellular  space,  but  are  not 
inclosed  in  capsules,  excepting  those  of  the  posterior  spinal  and  ver- 
tebral ganglia.  The  reason  for  this  is  that  within  the  central  nervous 
system  there  is  no  neurilemma  (nucleated  sheath  of  Schwann) ;  such 
sheath  being  found  in  the  peripheral  system  only. 

Marinesco  has  shown  by  studying  the  anatomy  of  the  fresh  nerve- 
cell  by  means  of  the  ultra  microscope  some  new  details  of  the  structure 


Fig.  7. — From  a  transverse  section  through  the  sciatic  nerve,  ep,  Epineurium; 
p,  perineurium;  n,  nerve  fibres  constituting  a  nerve  bundle  of  fasciculus  in  cross- 
section;/,  fat  tissue  surrounding  the  nerve.     (Klein.) 

of  the  cell.  The  body  of  the  cell  is  composed  of  a  complex  of  colloidal 
substances  whose  particles  are  illuminated  by  the  lateral  light  of  the 
ultra  microscope.  Fig.  6  shows  four  cells  taken  from  the  ganglion  of 
a  dog,  examined  in  the  serum  of  the  same  animal. 

The  nerve-cells  of  the  sympathetic  or  vertebral  ganglia  are  very 
like  the  central  nerve-cells  in  the  anterior  horns.  They  are  multipolar 
in  shape  and  have  dendrites  and  a  neuraxon.  The  neuraxon  goes 
to  other  neighboring  cells,  or  it  passes  on  to  the  spinal  cord  or  the  per- 
iphery. The  cell  is  surrounded  by  a  connective-tissue  capsule  lined 
with  a  flat  epithelium,  like  those  of  the  posterior  spinal  ganglia.  The 
peripheral  or  terminal  sympathetic  nerve-cells  lying  in  the  viscera 
resemble  those  of  the  vertebral  ganglia. 

Nerve-cells  are  classified  in  accordance  with  their  shape  and  num- 
ber of  processes.     The  multipolar  cell  is  the  common  type  and  is  found 


8  DISEASES    OF    THE    NERVOUS    SYSTEM 

throughout  the  bram,  cord,  and  sympathetic  gangha.  Bipolar  cells 
are  found  chiefly  in  the  column  of  Clark  of  the  spinal  cord  and 
in  spinal  ganglia.  Small  nuclear  cells  and  flask-shaped  or  Purkinje's 
cells  are  found  in  the  cerebellum.  Besides  these  there  are  described 
in  the  brain  cortex  angular,  granular,  pyramidal,  globose,  and  spindle- 
cells. 

The  nerve- fibres  of  the  nerve-centres  are  found  chiefly  in  the  white 
tissue  or  white  matter.  In  the  periphery  they  form  the  nerve  proper 
of  gross  anatomy.  The  peripheral  nerve  is  composed  of  bundles  of 
nerve-fibres  called  nerve  fasciculi  (Fig.  7).  It  is  surrounded  by  a  con- 
nective-tissue sheath  called  the  sheath  of  Henle, 
or  epineurium.  From  this  sheath,  connective- 
tissue  fibres  pass  in  and  surround  the  fasciculi. 
The  sheath  of  the  fasciculus  is  called  the 
perineurium.  From  the  perineurium,  strands 
of  connective  tissue  run  in  among  the  ultimate 
nerve-fibres,  forming  the  endoneurium  (Figs.  8 
and  9) .  Lymphatic  spaces  lined  with  endothe- 
lium exist  in  the  layers  of  the  peri-  and  endo- 
FiG.  8.^A  simple  funic-  sheaths.  In  the  nerve-centres,  the  nerve- 
The  "SpplreLf  ^JmS'l^SS  ^^I'^s,  have  no  such  sheaths,  but  are  supported 
ated  cells  are  sections  of  the  by  a  connective  tissue  and  neuroglia  framework. 
?Xnd*"%:  Axi^'^iJiS;  The  nerve-fibre  is  a  long  fine  strand  of  tie- 
10,   white    substance    of  sue  varying  in  diameter.     It  may  be  white  or 

litZTn,  neunlltaTer^el;:  8™y..  '^'^'^o-'ding  to  whether  it  has  or  has  not  a 

doneurium;  p,  perineurium;  myelin  sheath.  It  is  composed  from  within  out 
tiesZT7fl^Z)""^^'  °^  Of   (1)   an  axis-cyhnder,    (2)   a  myelin  sheath, 

and  (3)  a  neurilemma.  (1)  The  axis-cylinder 
is  the  essential  part  of  the  nerve.  It  is  the  prolongation  of  the  neu- 
raxon  of  a  nerve-cell  and  consists  of  protoplasm.  It  is  itself  made  up  of 
fine  fibrillse  (primitive  fibrillse)  which  run  longitudinally. 

The  myehn  sheath  is  developed,  hke  the  axis-cylinder,  from  the 
ectoderm,  and  is  closely  related  nutritionally  to  the  axis-cylinder,  which 
it  protects  and  isolates.  (3)  The  neurilemma  or  nucleated  sheath  is  a 
dehcate  covering  forming  the  outermost  sheath  of  the  nerve.  It  is 
also  of  ectodermic  origin.  The  sheath  is  absent  in  the  fibres  of  the 
central  nervous  system  and  in  some  fibres  of  the  periphery. 

Variations  in  the  Types  of  Fibres.- — In  accordance  with  the  arrange- 
ment of  the  sheaths  of  the  nerve-fibres,  several  kinds  are  described. 
The  principal  types  are  the  medullated  and  non-medullated. 

Medullated  nerve-fibres  make  up  the  bulk  of  the  white  matter  of  the 
brain  and  cord  and  cerebrospinal  nerves.  They  consist  of  a  mj^elin 
sheath  and  axis-cylinder,   and  may  or  may  not  have  a  neurilemma. 


GENERAL    ANATOMY,    PHYSIOLOGY,    AND    CHEMLSTRY  9 

Fibres  with  myelin  sheath,  but  without  a  neurilemma,  make  up  the 
white  matter  of  the  central  nervous  system. 

Non-medullated  fibres,  or  fibres  of  Remak,  occur  principally  in  the 
sympathetic  system,  but  they  are  also  found  in  the  cerebrospinal  nerves. 
They  are  grayish  and  faintly  striated,  and  consist  of  axis-cylinders, 
with  a  thin,  homogeneous,  nucleated  sheath,  the  neurilemma,  lying  directly 
upon  them. 

Naked  axis-cylinders  are  found  in  the  peripheral  terminations  of 
nerves  as  well  as  in  the  brain  and  cord  and  sympathetic. 

Size. — The  nerve  fibres  are  of  two  kinds  as  regards  size.  The  small 
fibres  are  about  2ijl  or  M2000  inch  in  diameter,  the  large  20 fx  or  M200 
inch.  The  small  fibres  are  connected  with  smaller  cells,  and  either 
run  a  shorter  course  or  are  distributed  to  the  involuntary  muscular 


X 


,  ■::% 


Fig.   9. — iSeetion  of  nerve.      {Quain.) 

fibres  of  the  blood-vessels  and  viscera.  The  motor  fibres  are  larger 
than  the  sensory. 

The  white  fibres  of  the  sympathetic  nervous  system  are  about  one- 
third  smaller  than  the  ordinary  cerebrospinal  or  somatic  fibres. 

The  peripheral  nerve-fibres,  except  the  optic,  have  no  neuroglia; 
they  terminate  in  fine  fibrillae  among  epithelial  cells,  or  in  special  end- 
organs. 

The  central  nervous  fibres  make  up  the  white  matter  of  the  brain  and 
cord.     They  are,  like  the  peripheral  nerves,  the  prolongations  of  the 


10 


DISEASES    OP    THE    NEEVOUS    SYSTEM 


neuraxons.  They  are  composed  of  an  axis-cylinder  process  and  myelin 
sheath,  but  have  no  neurilemma,  and  probably  no  nodes.  At  fre- 
quent intervals  each  fibre  gives  off  branches  at  right  angles  forming 
the  "collaterals." 

Connections  of  Nerve-cells  and  Nerve-fibres. — One  nerve-cell  is 
never  connected  directly  with  another,  so  far  as  anatomical  investiga- 
tion can  show.  One  nerve  process  becomes  an  axis-cylinder,  receives  a 
myelin  sheath,  gives  off  collaterals,  and  finally  breaks  up  into  a  fibrillary 
"end-brush"  surrounding  a  cell,  but  not  passing  into  it.  There  is 
physiological,  but  no  apparent  anatomical  continuity. 


Fig.    10.  Fig.  11.  Fig.  12. 

Fig.  10. — MeduUated  nerve  fibre,  a,  Axis  cylinder;  n,  nucleus;  m,  medullary 
sheath;  c,  node  of  Ranvier. 

Fig.  11. — MeduUated  nerve  fibre,  showing  mode  of  division. 
Fig.  12. — -Non-meduIIated  nerve  fibre,     n,  Nucleus;  6,  striations. 

The  Neuroglia. — The  supporting  tissue  of  the  peripheral  nerves 
is  connective  tissue  only;  that  of  the  central  nervous  system  is  con- 
nective tissue  and,  in  addition,  a  peculiar  substance  called  neuroglia. 
The  neuroglia  or  supporting  tissue  of  the  nervous  centres  is  derived 
from  the  ectoderm.  It  is  composed  of  cells  with  very  numerous  and 
finely  ramified  processes,  which  make  a  supporting  network  about 
the  nerve-cells  and  fibres  (Fig.  13).  The  cell-body  is  composed  of 
granular  protoplasm,  lying  in  which  is  a  large  nucleus,  within  which  is 
the  nucleolus.  The  body  of  the  cell  is  small  in  amount  in  proportion 
to  the  nucleus.     The  fibrillary  processes  form  a  felt-like  network,  and 


GENERAL   ANATOMY,    PHYSIOLOGY,    AND    CHEMISTRY 


11 


in  regions  where  there  is  much  neurogHa  tissue  this  looks  like  a  homo- 
geneous matrix.     It  is,  however,  made  up  of  the  fine  fibrils. 

The  Non-nervous  Tissue — The  Blood-vessels. — The  peripheral  nerves 
are  richly  supplied  with  blood.     Each  nerve  receives  arterial  supply 


Fig.  13. — Phases  in  the  development  of  neuroglia  cells  and  fibrils.  lA,  Divid- 
ing neuroglia  nuclei  surrounded  by  protoplasm;  2B,  protoplasmic  processes  more 
definitely  formed;  3C,  commencing  condensation  of  protoplasmic  processes  producing 
darkly  staining  fibril;  4Z)  and  5E,  mode  of  attachment  of  the  processes  to  a  vessel 
wall  and  differentiation  of  foot  into  fibrils;  QF,  further  development  of  fibrils;  7G, 
protoplasm  almost  entirely  differentiated  into  fibrils  and  nucleus  shrunken.  (From 
figures  drawn  by  Dr.  George  A.  Watson.) 


from  many  different  branches,  but  always  from  the  same  general  source. 
The  artery  passes  to  the  nerve-sheath  obliquely,  then  divides  dichoto- 
mously  and  sends  branches  a  long  distance  up  and  down  on  the  sheath. 
It  may  pierce  the  sheath,  however,  first,  and  then  divide,  as  above  de- 


12 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


scribed.  The  dichotomous  branches  send  off  arterioles  and  capillaries, 
which  form  plexuses  about  the  nerve  fascicles.  These  are  "the  inter- 
fascicular arcades."  The  arteries  subdivide  in  such  a  way  as  to  pre- 
vent sudden  impact  of  a  large  bloocl-stream  into  the  tissue  of  the  nerve. 
In  this  respect  the  nerve  circulation  resembles  that  of  the  brain  and  cord. 
The  veins  subdivide  dichotomously,  like  the  arteries.  They  freely 
anastomose  with  the  muscular  veins,  so  that  muscular  action  helps  nerve 
circulation.  The  veins  of  the  superficial  nerves  connect  with  those  of 
the  deep  nerves. 

The  blood-vessels  of  the  spinal  cord  and  brain  will  be  described  later. 


Fig.  14. — Glia  cells  as  impregnated  in  silver-chromate  preparations. 
(After  Ramon  Cajal.) 

Lymphatic  vessels  and  spaces  are  found  in  the  epineurium  and 
perineurium.  There  are  no  distinct  lymphatics  in  the  fasciculi,  but 
lymph-spaces  probably  exist. 


THE  NEURONIC  ARCHITECTURE  OF  THE  NERVOUS  SYSTEM 

Having  described  the  component  parts,  I  shall  now  show  the  way 
in  which  these  parts  are  arranged  to  form  the  nervous  system. 

The  nervous  system,  as  already  shown,  is  composed  of  single  nerve 
units  that  are  called  neurons,  and  the  neuron  is  made  up  of  a  cell-body 
and  numerous  processes,  one  of  which  is  the  neuraxon,  the  others  the 
dendrites. 


GENERAL    ANATOMY,    PHYSIOLOGY,    AND    CHEMISTRY  13 

The  neuraxon  has  always  the  function  of  carrying  impulses  away 
from  the  cell;  it  is  a  cellufugal  fibre;  the  dendrites,  however,  bring 
impulses  to  the  cell,  and  are  cellupetal  in  function.  The  dendrites 
are  in  contact  with  end-brushes  or  end-buds  of  the  neuraxons  of  other 
cells,  and  in  this  way  receive  the  nerve  impulse  and  transmit  it  to  the 
cell-body.  The  nervous  system  is  thus  a  mass  of  neurons  which  are 
packed  closely  together,  and  form  with  each  other  most  intricate  rela- 
tions, but  never  connect  directly  one  with  another.  No  nerve-fibre 
or  dendrite  of  one  cell  anastomoses  with  that  of  another,  as  blood-vessels 
do.     Each  neuron  is  anatomically  independent. 

It  is  the  purpose  of  this  neuronic  mass  to  receive  impulses  from 
within  or  without  the  body,  to  transfer  and  modify  them,  and  to  send 
out  impulses  in  such  way  as  properly  to  control  the  vital  functions 
and  keep  the  individual  in  proper  harmony  with  his  environment. 
The  nervous  system  is  a  great  receiving,  regulating,  controlling,  and 
discharging  machine,  the  machinery  being  the  neurons,  the  force  that 
works  in  it  being  called  nervous  energy.  The  neurons  as  a  whole  have 
this  force  stimulated  or  aroused  in  them.  The  nerve-cell  co-ordinates  and 
distributes  it.  The  nerve-cells  are  massed  together  for  the  most  part  in 
the  brain  and  spinal  cord,  forming  the  gray  matter,  while  the  neuraxons 
as  distributors  make  up  the  white  matter  and  the  cranial,  spinal,  and 
sympathetic  nerves.  It  is  convenient  to  make  a  division,  therefore, 
into  the  central  or  somatic  nervous  system,  with  its  peripheral  nerves, 
cranial  and  spinal,  and  the  sympathetic  or  autonomous  nervous  system. 

The  Somatic  Nervous  System. — Since  the  nerve-fibres  of  the  brain  and 
cord  are  white  in  texture,  while  the  cells  in  mass  are  of  gray  color,  it  is 
very  easy  to  distinguish  the  deposits  of  cells  from  the  fibres  and  thus 
make  subdivisions  of  the  central  nervous  tissue.  One  portion  of  this 
gray  matter  is  found  deposited  in  the  centre  of  the  spinal  cord,  extending 
up  to  the  floor  of  the  medulla,  thence  underneath  and  around  the  aqueduct 
of  Sylvius  to  the  floor  of  the  third  ventricle.  This  is  called  the  central 
gray  matter.  Another  deposit,  much  larger  in  amount,  covers  the  whole 
of  the  cerebrum  and  cerebellum,  and  forms  the  cerebral  and  cerebellar 
cortex.  Smaller  deposits  make  up  the  great  hasal  ganglia,  corpus  striatum, 
optic  thalamus,  and  corpora  quadrigemina,  besides  several  small  deposits 
(the  small  hasal  ganglia  cerebral  and  cerebellar),  such  as  Luys'  body, 
the  red  nucleus  and  Deiter's  nucleus. 

The  peripheral  nervous  system  contains  nerve-cells,  as  well  as  fibres. 
Their  anatomical  arrangement  is  easily  understood,  but  their  relation 
to  the  central  nervous  system  is  less  simple. 

The  sy?npathetic  nervous  system  consists  of  (A)  an  autonomic  or 
parasympathetic  portion  and  (B)  a  sympathetic  system  proper    (Fig.  15). 

The  autonomic   nervous   system   is   in   general  distinguished  from 


14 


DISEASES    OF   THE    NERVOUS   SYSTEM 


the  sympathetic  proper  by  the  fact  that  it  does  not  at  first  pass  into 
any  ganghon,  but  runs  in  cranial  or  spinal  nerves  until  it  reaches  the 
periphery.  It  then  enters  a  ganglionic  mass,  and  from  this  it  sends  fibres 
to  the  peripheral  organ. 

(A)  This  autonomic  system  consists  of  a  mid-brain,  a  hind-brain 


Fig.  15. — Scheme  of  the  autonomic  and  sympathetic  system  proper,  according  to 

Langley. 


and  a  sacral  portion.  The  mid-brain  autonomic  system  sends  out 
fibres  which  run  into  the  third  nerve  to  the  ciliary  ganglion  and  thence 
fibres  to  the  ciliary  muscles  and  the  sphincter  of  the  iris. 

The  hind-brain  autonomic  system  sends  fibres  which  run  into  the 
nerve  of  Wrisburg  and  the  seventh  nerve;  the  glossopharyngeal  and  the 
vagus.     The  fibres  that  run  in  the  nerve  of  Wrisburg  and  the  seventh 


GENERAL   ANATOMY,    PHYSIOLOGY,    AND    CHEMISTRY 


15 


nerve  go  to  the  submaxillary  and  the  sublingual  ganglia  and  thence 
supply  the  vasodilator  nerves  to  the  tongue,  submaxillary  and  sub- 
lingual glands  and  secretory  fibres  and  vasomotor  fibres  to  the  mucous 
membrane  of  the  nose,  soft  palate  and  upper  pharynx. 

It  sends  fibres  via  the  glossopharyngeal  nerve  to  the  otic  ganglion 
and  these  control  secretion  and  vasodilation  in  the  parotid  gland. 

The  most  important  parts  of  the  hind-brain  autonomic  fibres  run  in 
the  vagus  nerve.  They  go  to  the  jugular  ganglion  and  the  ganglion 
of  the  trunk  and  of  the  vagus  and  thence  send  motor  and  secretory 
fibres  to  the  oesophagus,  stomach  and  small  intestines,  as  far  as  the  ileo- 
cecal valve. 

The  sacral  autonomic  system  consists  of  fibres  which  pass  out  through 
the  second  and  third  sacral  nerves  and  are  connected  with  the  ganglia 
of  the  hypogastric  plexus.  They  send  fibres  which  supply  motor  fibres 
to  the  bladder  and  colon  and  rectum,  inhibitory  fibres  to  the  sphincter 
of  the  bladder  and  rectum. 

In  a  general  way  it  is  found  that  the  autonomic  and  sympathetic 
systems  antagonize  each  other  in  their  action,  thus  the  fibres  of  the  au- 
tonomic system  contract  the  pupil;  those  of  the  sympathetic  dilate; 
the  fibres  of  the  hindbrain  of  the  autonomic  system  inhibit  the  heart 
and  stimulate  movement  and  secretion,  while  the  sympathetic  fibres 
antagonize  this  action.  The  same  is  true  though  to  a  less  marked  extent 
of  the  sacral  portion  of  the  autonomic  system. 


Autonomic  or  Para-sympathetic. 


Mid-brain  portion. 
Bulbar  portion. 


Sacral  portion. 


Contracts  pupil. 
Coronary  blood-vessels. 
Inhibits  heart-action. 
Dilates  blood-vessels. 
Inhibits  sweat-glands. 
Contracts     muscle-walls     of 

cesophagus, 

cardiac  sphincter, 

stomach. 
Stimulates  gastric-secretion. 
Dilates  blood-vessels  of 

rectum, 

anus. 

external  genitals. 
Contracts  muscles  of  colon, 

rectum, 

anus, 

external  genitals, 

bladder, 

urethra. 


Sympathetic. 

Dilates  pupil. 
Coronary  blood  vessels. 
Accelerates  heart-action. 
Contracts  blood-vessels. 
Stimulates  sweat-glands. 
Relaxes   muscle-walls  of 

oesophagus, 

stomach, 

cardiac  sphincter, 

Contracts  blood-vessels  of 

rectum, 

anus. 

external  genitals. 
Relaxes  same 


16  DISEASES    OF    THE    NERVOUS    SYSTEM 

(B)  The  sympathetic  system  proper  consists  of  the  two  chains  of 
vertebral  gangha,  of  their  peripheral  ganglia  (cceliac,  etc.),  and  of  con- 
necting fibres. 

Both  portions  of  the  sympathetic  system  have  efferent  and  afferent 
fibres.  The  efferent  nerves  never  pass  directly  to  the  tissue  to  be  in- 
nervated, but  first  go  to  ganglia,  from  which  a  second  neuron  sends  out 
its  fibres  to  the  terminal  organ  or  gland. 

The  afferent  or  sensory  fibres  are  very  few  compared  with  the  efferent, 
so  that  the  viscera  have  no  sensibility  except  on  great  and  peculiar 
irritation.  The  sensations  evoked  reach  the  cord  but  the  brain  and 
consciousness  are  reached  through  the  somatic  sensory  fibres  which  in 
general  refer  the  pain  to  the  corresponding  somatic  segments. 

The  sympathetic  fibres  to  the  viscera  run  mostly  as  independent 
nerves,  but  the  fibres  to  the  trunk  and  extremities  and  head  run  mostly 
in  the  trunks  of  the  somatic  nerves. 

I  come  now  to  a  description  of  the  general  arrangement  of  these 
various  nerve  units;  and  here  I  must  suppose  that  my  reader  has  a 
knowledge  of  the  ordinary  anatomy  of  the  subject. 

The  nerve-cells  of  the  ganglia  on  the  posterior  spinal  roots  fur- 
nish the  best  starting-point  in  an  attempt  to  trace  out  the  connections. 
These  cells  give  off  a  single  process,  which  quickly  divides  in  a  T  shape. 
One  branch  of  the  T  passes  peripherally  through  a  mixed  spinal  nerve 
to  the  skin,  forming  a  sensory  nerve.  The  other  passes  centrally,  enters 
the  posterior  spinal  roots,  and  breaks  up  into  little  filaments,  which 
surround  a  nerve-cell  in  the  posterior  horn  or  analogous  nuclei.  This 
forms  the  first  or  outer  sensory  neuron.  The  outer  branch  of  the  spinal 
ganglion  cell  which  went  to  the  periphery  as  a  sensory  nerve  was  its 
dendrite,  or  protoplasmic  process,  which  has  evolved  into  a  sensory  nerve 
and  is  cellwpetal  in  function.  The  other  process  is  the  neuraxon  proper 
and  it  is  cellufugal,  carrying  impulses  away  from  the  ganglion  cell  into 
the  cord. 

The  next  neuron  begins  as  a  cell  in  the  posterior  horn,  or  in  like 
parts.  It  sends  a  neuraxon  up  the  spinal  cord,  a  collateral  branch 
passes  to  the  cerebellar  cortex,  while  the  direct  fibre  surrounds  a  cell 
in  the  optic  thalamus.  This  forms  the  second  sensory  neuron.  The 
cell  in  the  thalamus  gives  off  a  neuraxon  which  passes  to  the  gray  matter 
of  the  cerebral  cortex,  and  here  it  either  directly  affects  the  cells  in 
this  region  or  does  it  through  the  medium  of  another  shorter  neuron, 
which  is  called  ''associative." 

Thus  each  sensory  impulse  from  the  periphery  reaches  the  con- 
scious centres  of  the  brain  by  passing  along  three  or  four  neurons.  The 
primary  neuron  in  all  cases  lies  mainly  outside  the  central  nervous 
system  and  forms  a  sensory  nerve.     The  sensory  nerves  do  not  there- 


GENERAL    ANATOMY,    PHYSIOLOGY,    AND    CHEMISTRY 


17 


fore  arise  in  the  cord  or  medulla,  but  have  their  terminal  nuclei  there. 
Afferent  nerves  serve  the  purpose  of  conducting  impulses  which  arouse 
sensation,  and  reflex  action. 

The  sensory  nerves  of  the  surface  of  the  body  are  called  extero-ceptive 
when  they  excite  reflex  action.  They  are  more  closely  associated  with 
the  cerebrum  and  the  activity  of  the  skeletal  muscles.  The  visceral 
nerves  which  excite  reflexes  are  called  proprio-ceptive.  Thej"  are  asso- 
ciated with  the  cerebellum,  and  the   visceral  muscles.     They  give  rise 


''':_  A.Jifei/ron  _y 

Fig.  16. — Diagram  showing  the  arrangement  of  the  neurons  or  nerve  units  in  the 
architecture  of  the  nervous  system.  M.  Neurons  I.  and  II.,  Motor  neurons;  S.  Neu- 
rons I.,  II.,  III.,  sensory  neurons;  A.  Neuron,  associative  or  commissural  neuron. 


to  the  tonic  reflex  which  keeps  the  voluntary  muscles  at  a  certain  degree 
of  tension  (Sherrington).     (See  also  Fig.  18  p.  33.) 

The  neurons  of  the  brain  cortex  cannot  yet  be  distinctly  classi- 
fied, and  I  shall  not  attempt  it  here  at  all.  The  matter  will  be  brought 
out  more  fully  in  connection  with  the  anatomy  of  the  brain.  It  is 
sufficient  to  say  that  nerve  units  connect  together  the  cerebellum  and 
cerebrum  with  the  basal  ganglia,  the  frontal  lobes  and  the  cerebellum, 
the  two  hemispheres  of  the  cerebrum,  and  different  areas  of  the  cerebral 
cortex.  Leaving  out  of  consideration  these  neurons,  which  are  largely 
psychic  in  function,  we  start  with  the  large  motor  cells  in  the  central 

2 


18  DISEASES    OF    THE    NEKVOUS    SYSTEM 

convolutions  of  the  brain.  These  send  down  neuraxons,  which  pass 
into  the  spinal  cord  and  surround  the  cells  of  the  anterior  horns.  They 
form  the  upper  or  central  motor  neurons.  The  anterior  horn-cells 
send  off  neuraxons,  which  pass  out  through  the  anterior  roots  and  thence 
to  the  voluntary  muscles.  These  are  the  lower  or  peripheral  motor 
neurons.  These  motor  neurons  have  a  double  function — that  of  excit- 
ing muscles  to  contract,  and  that  of  inhibiting  muscular  activity  and 
causing  them  to  relax.  The  efferent  nerves  are  almost  equally  inhibitory 
and  motor.  With  each  voluntary  muscular  act  impulses  to  contract, 
excite  for  example  the  flexor  groups,  and  impulses  to  relax,  cause  the 
opposing  extensors  to  relax.  ^The  motor  mechanism  is  a  motor-in- 
hibitory mechanism.  This  has  been  especially  established  by  Professor 
Sherrington.  Besides  this  there  are  groups  of  cells  in  the  lateral  horns 
and  central  parts  of  the  spinal  cord  which  send  off  neuraxons  that  also 
pass  through  the  anterior  root,  but  they  leave  the  cerebrospinal  nerves 
and  enter  the  vertebral  sympathetic  ganglia.  Here  they  in  part  surround 
the  cells  of  these  ganglia  and  have  their  terminals  there.  These  sym- 
pathetic ganglion  cells  in  turn  send  neuraxons,  which  pass  in  the  sym- 
pathetic nerves  to  the  peripheral  ganglia,  where  they  meet  a  third  group 
of  neurons.  They  also  connect  with  the  other  gangha  of  their  own 
class  and  send  neuraxons  through  the  posterior  spinal  roots  to  the 
cord.  It  is  not  known  with  what  neurons  higher  up  in  the  nerve-cent- 
res the  lateral  horn-cells  are  connected,  but  probably  with  cells  in  the 
thalamus. 

Such  in  outline  is  the  neuronic  architecture  of  the  nervous  system. 
I  do  not  attempt  here  to  work  out  the  neurons  of  the  special  senses, 
nor  to  introduce  the  spinal  cerebellar  neuron.  This  will  be  done  later. 
It  is  sufficient  to  say  that  the  studies  in  this  direction  show  a  marvellous 
harmony  as  well  as  beauty  in  nature's  scheme. 

The  neuronic  architecture  is  shown  in  the  accompanying  diagrams 
(Figs.  16  and  18). 

GENERAL  PHYSIOLOGY 

The  Peripheral  Neurons. — The  nerves  which  run  between  nerve- 
centres  and  end-organs  carry  impulses  each  way.  They  are,  therefore, 
divided  into  the  afferent,  centripetal  or  ingoing,  and  efferent,  centrifu- 
gal or  outgoing.  The  old  division  into  motor  and  sensory  nerves  will 
not  answer,  for  there  are  many  outgoing  nerves  which  are  not  motor. 
The  afferent  nerves  are: 


GENEEAL   ANATOMY,    PHYSIOLOGY,    AND    CHEMISTRY  19 

1.  The  sensory,  including: 


These  carry 

(a)  Epicritic    sensations 

and 
(6)  Protopathic  sensa- 
tions. 


Nerves  of  general  /  Pain  nerves  or  pathic    nerves,   heat 
sensation.  \      and  cold  or  thermic  nerves. 

f  Contact, 
Tactile,  including  {  Pressure, 
[  Locality. 

Nerves  of  special      ,-,  ^  ,  ,        ,  •     , 

^.  <   Nerves    or    muscular    and    articular 

sensation. 

sense. 

Nerves  of  special  sense  of  smell,  sight, 

taste,  hearing  and  space. 

_    „     .^        „  Extero-ceptive. 

2.  Excito-renex  nerves.  {  „  ^ . 

[  rropero-ceptive. 

Protopathic  and  Epicritic  Sensibility. — According  to  Dr.  Henry  Head, 

the  afferent  nervous  system  is  composed  of  two  different  sets  of  sensory 
fibres,  called  the  protopathic  and  the  epicritic. 

The  protopathic  set  or  system  which  is  distributed  to  the  skin  and 
viscera,  and  to  the  muscles. 

(a)  The  fibres  to  the  skin  run  in  the  peripheral  nerves  and  give 
to  it  a  low  degree  of  sensibility.  The  fibres  to  the  viscera  run  in  the 
sympathetic  and  give  to  it  also  a  low  degree  of  sensibility. 

(b)  A  set  of  deep  fibres  to  the  muscles  which  supply  the  sense  of 
deep  pressure.  These  fibres  run  in  the  muscular  nerves  and  are  con- 
nected with  the  Paccinian  bodies. 

The  "protopathic  system,"  then,  as  a  whole,  consists  of  fibres  of 
sensibility  which  supply  the  skin,  the  viscera,  and  all  parts  of  the  body, 
inside  and  out.  It  furnishes  a  low  degree  of  sensibility  to  the  viscera, 
muscles  and  to  the  skin.  This  system  enables  one  to  appreciate  a  sense 
of  pain  and  temperature,  though  not  to  a  very  delicate  extent. 

There  is  another  system  of  .afferent  fibres  which  supply  the  skin 
alone,  a  purely  cutaneous  system,  and  this  is  called  epicritic.  This 
epicritiw  sensibility  enables  us  to  appreciate  light  touch,  the  points  of 
the  cornpass,  localization,  and  minor  degrees  of  temperature,  ranging 
between  22°  and  40°C. 

Epicritic  sensation  gives  us  the  sense  of  the  point  (a  variant  of  ap- 
preciation of  relative  size). 

Protopathic  sensation  gives  sense  of  pain  apart  from  the  knowl- 
edge of  the  pain-producing  object. 

The  epicritic  fibres  furnish  a  delicate  and  localized  appreciation 
of  pain.  Protopathic  fibres  carry  sensations  which  are  badly  local- 
ized, widely  diffused  and  sometimes  referred  to  other  parts  than  that 
of  the   stimulation.     The   protopathic   fibres   are  incapable   of   appre- 


20  DISEASES    OF    THE    NERVOUS    SYSTEM 

elating  light  touch,  and  minor  degrees  of  heat  and  cold,  and  pain 
appreciation  is  a  diffuse  tingling  and  thrilling  sensation.  This  distri- 
bution of  sensory  fibres  exists  only  in  the  peripheral  nerves.  In  the 
nerve-roots  and  central  nervous  system  the  systems  are  fused.  [The 
above  description  of  the  views  of  Dr.  Head  and  his  associates  has 
been  seen  and  corrected  by  Dr.  Head,  of  whose  courtesy  I  make 
acknowledgment.] 

The  efferent  nerves  are: 

1.  Motor  nerves,  going  to  voluntary  or  striped  muscles,  heart  muscle, 
smooth  muscle,  including  the  vasoconstrictor  and  dilator  nerves. 

2.  The  secretory.  These  act  upon  glands.  Impulses  to  the  blood- 
vessels (vasomotor)  generally  accompany  the  secretory  impulses. 

3.  The  inhibitory.  These  nerves  control  muscular  movements, 
secretion,  perhaps  also  nutrition. 

Central  Neurons. — There  are  intercentral  or  associative  neurons, 
which  connect  different  parts  of  the  cerebrospinal  system  together. 
Some  of  these  connect  symmetrical  parts  on  each  side  together  and 
have  a  coordinating  function.  Others  connect  higher  with  lower  centres 
and  carry  ascending  and  descending  impulses. 

End  Organs. — In  the  peripheral  nervous  system  we  have  end-organs. 
These  are  delicate  and  in  some  cases  complex  arrangements  of  nervous 
and  other  tissue  at  the  periphery  of  the  nerves.  Their  object  is  to  allow 
the  nerves  to  be  irritated  by  special  stimuli  which  would  not  otherwise 
affect  them,  e.g.,  light  or  sound.  Their  object  is  also  the  proper  utiliza- 
tion of  efferent  impulses  upon  other  tissues.  There  are  end-organs, 
therefore,  for  both  sensory  or  afferent  and  for  efferent  nerves.  The 
end-organs  of  the  afferent  nerves  are — eye,  ear,  taste-buds,  corpuscles 
in  the  Schneiderian  membrane,  various  tactile  cells  and  bodies,  the 
space  sense-organ,  the  muscle-spindles. 

For  the  efferent  nerves — neuro-muscular  corpuscles  in  the  vol- 
untary muscles,  local  ganglia  about  the  arteries,  local  ganglia  in  the 
glands.  Trophic  end-organs  are  not  known.  In  many  cases  the  end- 
organ  is  nothing  but  the  terminal  fibre  of  the  nerve.  This  loses  both 
medullary  sheath  and  neurilemma,  leaving  only  the  axillary  cylinder. 
It  then  splits  up  into  a  terminal  plexus,  or  else  without  splitting  passes 
between  and  around  the  cells  which  it  is  to  affect. 

The  Work  of  the  Cell-body  of  the  Neuron. — In  the  working  of  these 
mechanisms  the  nerve-cell  body  is  the  agent  which  in  some  instances 
generates,  but  more  generally  distributes  and  directs  the  impulses  which 
pass  to  it.  The  larger  the  nucleus  of  the  cell  in  proportion  to  its  proto- 
plasmic body,  the  more  stable  or  less  sensitive  the  cell.  The  larger  the 
amount  of  protoplasm  relative  to  the  nucleus,  the  more  active  the  dis- 
charging power  of  the  cell.     The  nucleus  is  the  part  of  the  cell-body  which 


GENERAL   ANATOMY,    PHYSIOLOGY,    AND     CHEMISTRY  21 

is  essential  to  constructive  metabolism.  By  means  of  it  the  cell  builds 
up  its  protoplasmic  substance.  When  the  nucleus  dies,  the  cell  may  live 
or  function  for  a  time,  but  it  lives  only  on  what  has  been  stored  up;  it 
can  build  no  more  and  soon  dies.  Nerve-cells  with  few  exceptions 
(spinal  ganglia)  have  no  centrosomes;  they  cannot  divide  and  multiply. 
Once  dead  they  cannot  be  restored. 

The  nerve-fibres  conduct  impulses  variously  generated.  These  im- 
pulses travel  at  the  rate  of  about  100  to  120  feet  per  second.  It  is 
less  in  visceral  nerves  (25  to  30  feet  per  second).  Nerve-cells  are  ex- 
hausted by  successive  stimulations,  but  nerve-fibres  can  be  continually 
excited  and  are  practically  non-fatiguable.  There  are  no  electrical 
currents  in  normal  living  nerves  (Landois)  except  when  an  impulse  travels 
along  them.  Then  an  electrical  current  travels  along  with  the  im- 
pulse. It  is  called  the  current  of  negative  variation.  The  irritability 
or  excitability  of  a  nerve  is  the  power  it  has  of  responding  to  a  stimulus. 
When  a  constant  electrical  current  is  passed  along  a  nerve  its  irritability 
is  modified.  This  modified  condition  is  called  electrotonus.  When  a 
nerve-impulse  passes  up  an  afferent  nerve  and  is  then  reflected  along 
an  efferent  nerve,  it  is  called  a  reflex  action.  The  time  required  for  this 
process  is  called  the  reaction  time.  This  averages  from  0.125  to  0.2  of 
a  second. 

CHEMISTRY 

The  specific  gravity  of  nervous  tissue  is  about  1.036;  that  of  the 
brain  is  1.038;  of  the  spinal  cord  and  nerves,  1.034  (Bischoff,  Krause). 
The  reaction  is  alkaline,  but  this  is  lessened  by  activity,  owing  to  the 
development  chiefly  of  lactic  acid.  The  gray  matter  is  less  alkaline 
than  the  white. 

The  nervous  system  has  the  following  composition  (Baumstark, 
quoted  by  Hammarsten) : 

White  Matter  Gray  Matter 

Water  in  1,000  parts 695.35  769.97 

Solids 304.65  230.03 

T,     .  I  Cerebrin  1  ^  ^  , ,  „  ^ 

ProtagoiK^  } 25.11  10.08 

[  Lecethm  (neurm)  J 

Insoluble  albumin  and  connective  tissue 50 .  02  60 .  79 

Cholesterin 45 .  12  23 .  81 

Nuclein 2.94  1.99 

Neurokeratin 18 .  93  10 .  43 

Inorganic  salts 5 .23  5 .  62 

Water  makes  up  nearly  three-fourths  of  nervous  tissue,  there  being 
more  in  the  gray  than  in  the  white  matter  and  least  in  the  sympathetic 
nerves.  The  inorganic  salts  amount  to  about  0.5  per  cent.  The  largest 
single    constituent   is   phosphorus    (Breed)    combined    with    potassium, 


22  DISEASES     OF    THE    NERVOUS    SYSTEM 

sodium,  magnesium,   calcium,   and  iron,  forming  phosphate  salts.     Of 
the  other  constituents  chlorid  of  potassium  is  the  most  important. 

Protagon  is  a  very  complex  substance  of  a  fatty  character,  con- 
taining nitrogen  and  united  with  glycerin-phosphoric  acid  instead 
of  glycerin.  It  is  said  by  some  to  be  made  up  of  two  bodies,  cerebrin 
and  lecethin,  the  latter  containing  an  ammonia  compound  called  neu- 
rin.  Protagon  is  especially  found  in  the  white  matter.  The  gray 
matter  and  axis-cylinders  contain  globulins,  nucleo-proteid  and  nuclein, 
a  very  important  substance  in  cell  metabolism.  Nuclein  (C29H49N9P3O22, 
Miescher)  is  composed  of  nucleic  acid,  a  substance  rich  in  phosphorus 
and  a  variable  amount  of  albumin.  The  gray  matter,  i.e.,  the  nerve- 
cells,  contains  also  various  albuminous  substances.  Nucleo-keratin 
is  found  in  the  neuroglia  and  medullary  sheaths.  The  nuclein  and  the 
allied  substance  nucleo-albumin  are  called  albuminoids  (Halliburton). 
They  both  contain  phosphorus  and  are  found  chiefly  in  the  nucleus. 
The  albuminous  substances,  called  also  proteids  by  Halliburton,  have  little 
or  no  phosphorus,  and  make  up  the  most  of  the  cell-body  or  cytoplasm. 


CHAPTER  II 
THE  CAUSES  OF  NERVOUS  DISEASES 

Nervous  diseases  are  produced  in  part  by  predisposing  influences 
which  may  be  likened  to  a  fecund  soil;  in  part  they  are  due  to  exciting 
causes,  which  are  like  the  seeds  dropped  upon  the  soil  in  the  accidents 
of  life. 

Heredity  is  the  most  serious  and  important  of  these  predisposing 
causes,  in  particular  of  those  neuroses  that  are  constitutional  and  are 
not  the  results  of  bodily  accidents.  A  nervous  disease,  however,  is 
rarely  directly  inherited.  Parents  do  not  pass  down  special  maladies, 
but  only  a  general  tendency  to  nerve  disease,  which  is  not  developed 
into  any  distinct  trouble  unless  some  disturbing  cause  arises.  Nervous 
parents  may  have  children  who  have  unstable,  over-irritable,  and 
inadequate  nervous  systems.  Such  persons  have  what  is  called  a 
neuropathic  constitution  or  diathesis.  This  diathesis  may  be  transmitted 
when  the  parents,  though  not  especially  neurotic,  suffer  from  syphilis, 
alcoholism,  and  diseases  of  malnutrition,  like  tuberculosis.  So  far  as 
the  office  of  parentage  goes,  persons  of  great  talent  in  affairs,  or  great 
artistic  genius  in  any  direction,  may  be  counted  as  neurotic  and  are  very 
likely  to  have  children  of  neuropathic  constitution.  This  is  less  apt  to 
be  the  case  when  one  parent  is  of  stable  and  lymphatic  type.  If  two 
persons  having  not  simply  a  nervous  constitution  but  distinct  nervous 
or  mental  disease  marry,  their  children  are  liable  to  serious  nervous  or 
mental  disease.  The  intermarriage  of  blood  relations,  such  as  first  cous- 
ins, does  not  lead  to  neurotic  children,  if  the  parents  are  not  neurotic 
themselves,  and  are  of  robust  health  and  dissimilar  temperaments. 
Injuries  or  even  severe  shock  to  the  mother  during  the  early  months  of 
pregnancy  sometimes  leads  to  nervousness  in  the  offspring.  The  mother 
transmits  neuroses  more  often  than  the  father.  There  are  certain  rare 
nervous  diseases  which  appear  in  different  branches  and  members  of  a 
family,  such  as  an  uncle,  cousin,  nephew,  and  son.  These  diseases  may 
pass  also  by  direct  inheritance  from  parent  to  child,  or  may  skip  a 
generation.  They  are  called  "family  diseases,"  and  are  of  the  nature 
of  congenital  defects,  like  webbed  fingers  or  club-foot. 

Degeneration  is  the  name  given  to  a  condition  in  which  there  is  a 
morbid  deviation  from  the  normal  average  in  mental  traits,  physio- 
logical powers,  or  physical  structure.  It  is  a  term  most  often  used 
in   connection   with   mental   characteristics.     It   is   most   often   an  in- 

23 


24  DISEASES    OF    THE    NERVOUS    SYSTEM 

herited  state,  and  the  word  degenerate  is  often  used  to  indicate  a  person 
who  has  a  hereditary  neuropathic  or  psychopathic  constitution.  De- 
generacy in  a  moderate  degree  often  accompanies  great  mental  powers, 
especially  of  the  artistic  kind,  and  it  is  almost  invariably  associated  with 
genius.  It  is  quite  compatible  with  mental  soundness  and  a  fair  degree 
of  physical  health.  It  is  then  well  to  use  the  term,  suggested  by  Walton, 
of  deviation.  Those  who  have  unusual  mental  gifts  and  degenerate 
characteristics  are  called  superior  degenerates.  The  criminal  and  the 
insane  and  erratic  and  eccentric  persons  of  weak  judgment  have  also 
the  neurotic  constitution,  and  are  called  inferior  degenerates.  The 
weak-minded,  imbecile,  and  idiots  form  the  lowest  class  of  degenerates, 
and  are  called  the  dehiles.  Degeneracy  of  constitution  whether  inherited 
or  acquired  is  a  condition  which  fits  the  person  for  acquiring  nervous 
disease. 

Age. — In  infancy  and  early  childhood,  nervous  diseases  are  rather 
frequent  on  account  of  the  accidents  at  birth,  the  liability  to  infectious 
fevers,  and  malnutrition,  and  the  high  degree  of  sensitiveness  of  the 
yet  immature  nervous  system.  Still,  a  carefully  watched  infant  is 
relatively  safe.  Motor  disorders,  such  as  paralyses,  convulsions,  and 
chorea,  are  much  the  more  common  troubles.  At  the  time  of  puberty 
sensory  disorders,  such  as  headache,  and  migraine  appear,  and  often 
epilepsy,  hysteria,  and  disorders  of  sleep.  Hereditary  tendencies  to 
nervous  disease  also  begin  to  develop  at  this  time  or  a  little  later.  At 
the  period  of  adolescence,  the  maladies  already  mentioned  also  may 
be  brought  out;  but  in  addition  neurasthenic,  morbid  sexual,  hypo- 
chondriacal, and  insane  tendencies  are  seen.  From  maturity  to  the 
time  when  degenerative  changes  begin,  forty  to  forty-five,  the  indi- 
vidual suffers  from  those  nervous  disorders  brought  on  by  accidents', 
injuries,  prostrating  attacks  of  sickness,  over-strain,  infections,  in- 
dulgence in  alcohol  and  narcotics,  and  the  abuse  of  the  bodily  func- 
tions. At  and  after  the  climacteric,  one  sees  oftenest  such  maladies 
as  result  from  vascular  disease,  apoplexies,  brain  softening,  also  severe 
forms  of  neuralgia,  and  spasm. 

Sex. — Sensory  and  functional  disorders  are  more  frequent  in  women ; 
motor  and  organic  disorders  more  frequent  in  men. 

Condition  and  Occupation. — ^No  general  facts  will  be  laid  down 
here.  Celibates,  however,  it  may  be  said,  suffer  more  from  nervous 
disorders  than  married  people.  It  will  be  shown  later  that  certain 
occupations  entail  special  nervous  disorders  and  that  indoor  life  pro- 
motes functional  nervous  diseases. 

Work.^ — ^Hard,  constant,  excessive  muscular  work,  leads  to  arterial 
sclerosis  and  the  neuroses  that  result  from  a  defective  circulation. 

Mental  work  produces  no  injurious  effect  upon  metabolism  and  is  a 


THE    CAUSES    OF    NERVOUS    DISEASES  25 

healthful  form  of  activity,  even  intense  and  long-continued  mental  work 
being  comparatively  harmless.  It  is  the  worry  and  strain  and  emotional 
excitement  associated  with  hard  work  that  does  harm  and  leads  to 
neurasthenic  disorders. 

Mental  Attitude. — -The  expectant  and  untrained  mind  is  much  more 
liable  to  nervous  disease  as  the  result  of  injury,  shock,  etc.  Little  evil 
can  befall  a  prepared  mind.  The  Freudean  school  asserts  that  a  person 
who  has  been  ''analyzed"  is  much  less  subject  to  the  minor  psychoses. 

Habits. — Excessive  indulgence  in  alcohol  is  a  most  prolific  cause 
of  nervous  disease,  chiefly  by  the  action  of  this  substance  on  the  blood- 
vessels and  the  stomach.  Excesses  in  eating,  in  tea-drinking,  irregu- 
larity in  sleeping,  and  bad  habits  of  working  predispose  to  nervous  dis- 
ease. Sexual  excesses  are  usually  the  result  rather  than  the  cause  of 
nervous  disorders.  They  are  the  evidence  of  mental  more  than  of  nervous 
weakness.  Bad  mental  habits  acquired  usually  in  early  life  as  the  result 
of  wrongful  education  or  a  poor  environment  and  example  lead  to  many 
functional  nervous  disorders.  By  bad  mental  habits  is  meant  especially 
the  tendency  to  lay  too  much  stress  on  trivial  things,  to  worry  and 
"fuss"  over  details,  to  have  "precisions,"  to  get  "notions"  and  assume 
as  guides  in  life  foolish  types  of  religion,  philosophy  or  sanitation.  The 
obsessive  neurasthenic  is  one  of  the  characteristic  features  of  our  American 
civilization. 

Climate  and  Civilization. — Nervous  diseases  are  most  frequent  in 
temperate  climates,  and  in  those  which  are  dry  and  elevated.  They 
increase  with  the  progress  of  civilization  and  the  greater  strain,  com- 
plexity, and  luxury  of  modern  social  life.  Those  organic  nervous  dis- 
eases which  are  largely  dependent  on  vascular  disease  are  frequent  in 
the  poorer  classes,  among  whom  syphilis,  alcoholism  and  bad  feeding 
prevail.  Functional  and  degenerative  disorders  are  frequent  in  the  higher 
classes.  Nervous  diseases,  if  we  except  those  of  the  degenerative  type, 
prevail  more  in  urban  populations. 

Diathesis. — The  rheumatic  and  gouty  diatheses  predispose  to  nervous 
troubles,  more  especially  those  which  are  of  a  peripheral  and  functional 
nature.  Those  allied  conditions  in  which  the  products  of  tissue  waste 
are  not  properly  oxidized  and  eliminated,  have  a  similar  influence. 

Trauma  and  Shock. — Exhausting  hemorrhages  and  trauma  may  be 
the  direct  cause  of  or  may  predispose  to  nervous  disease.  Trauma 
and  mental  shock  may  cause  functional  diseases,  such  as  neurasthenia, 
or  may  lead  to  the  development  of  insanity  or  indirectly  to  degenerative 
organic  disease.  Mental  shock,  and  especially  a  fright,  oftener  than 
severe  bodily  injury,  leads  to  the  development  of  functional  neuroses. 
However,  it  is  only  the  weak,  the  neurotic  or  unprepared  who  can  be 
thus  affected. 


26  DISEASES    OF    THE    NEKVOUS    SYSTEM 

Infections. — In  comparison  with  their  frequency,  the  infective  fevers 
are  not  great  factors  in  producing  nervous  disease,  but  practically  they 
often  play  an  important  part.  Scarlet  fever  is  the  most  dangerous  dis- 
order in  this  respect.  Measles  perhaps  ranks  next;  then  follow  in- 
fluenza, diphtheria,  typhoid  fever,  and  pertussis.  Among  chronic  in- 
fections syphilis  ranks  first;  tuberculosis,  malaria,  the  pellagra,  and 
beriberi  are  also  to  be  mentioned.  The  importance  of  syphilis  which 
causes  perhaps  one-half  of  organic  nervous  diseases  will  be  dwelt  upon 
later. 

Poisons. — Tea,  coffee,  cocoa,  tobacco  and  lead,  mercury,  copper, 
and  arsenic,  are  to  be  placed  among  the  causes  of  nervous  disease. 
But  methyl  and  ethyl  alcohol  are  justly  credited  with  exerting  the  most 
sinister  influence  on  the  nervous  system  of  all  poisons.  Methyl  or  wood 
alcohol  is  a  deadly  poison  whether  drunk  or  inhaled  in  any  considerable 
amount. 

Ethyl  alcohol  is  generally  classed  among  the  narcotic  agents.  It 
has,  however,  a  primary  stimulating  effect  upon  the  organs  of  the  circu- 
lation, respiration  and  digestion,  and  also  upon  the  brain.  Its  effects 
vary  enormously  with  the  dose  and  with  the  constitution  of  the  patient. 
It  is  a  food  in  the  sense  that  about  90  per  cent,  is  used  up  in  the  body  and 
transformed  into  heat  and  energy,  like  sugar.  It  is  not,  however,  a  very 
good  food  under  ordinary  conditions,  but  it  can  be  used  as  such,  in  daily 
amounts  not  over  Bii  by  many  people,  after  adolescence. 

Alcohol  is  also,  correctly,  said  to  be  a  poison,  though  this  may  be 
said  of  almost  any  substance  that  is  taken  into  the  system,  if  used  to 
excess.  Alcohol,  however,  is  a  dangerous  poison  to  a  minority  of  people, 
either  because  they  cannot  use  it  temperately,  a  small  dose  leading  them 
at  once  to  excesses,  or  because  it  excites  and  disagrees  with  the  functional 
activities  of  the  system.  Alcohol  is  always  a  poison  when  taken  in  ex- 
cess and  in  some  people  a  small  amount  may  be  an  excess.  The  de- 
generate types  of  nervous  systems  are  very  sensitive  to  alcohol,  and  usu- 
ally made  worse  by  it,  so  that  the  use  of  it  by  degenerates  tends  to  make 
them  worse  and  extinguish  this  group  of  the  race. 

On  the  other  hand,  alcohol  by  intemperate  use,  can  lead  to  an 
acquired  degeneracy  in  healthy  constitutions.  History  shows  that 
both  those  races  which  indulge  excessively  in  alcohol  and  those  which 
do  not  use  it  at  all,  either  degenerate  or  do  not  progress.  Alcohol  causes 
a  small  percentage  of  epilepsy  through  inheritance,  and  a  still  smaller 
percentage  of  epilepsy  among  its  users.  It  is  a  large  factor  in  the  pro- 
duction of  acute  mental  disturbances,  such  as  delirium  tremens,  but 
not  a  large  factor  in  causing  degenerative  insanities  or  imbecility  or 
idiocy.  In  my  own  experience,  the  percentage  of  alcoholism  in  the 
ascendants  of  the  insane,  imbecile  and  idiotic,  is  about  5.     The  ratio 


THE    CAUSES    OF    NERVOUS    DISEASES  27 

of  insanity  to  the  population  is  about  the  same  in  prohibition  as  in  other 
states  in  this  country.  In  persons  who  inherit  degenerate  constitu- 
tions, that  is  to  say,  in  persons  with  a  weak  and  unstable  nervous  system, 
alcoholism  is  often  only  an  expression  of  this  instability,  not  a  cause  of 
it.  For  it  is  a  sign  of  degeneracy  to  drink  alcohol  to  excess  or  to  have  a 
morbid  susceptibility  to  its  effects. 

Alcohohsm  and  habits  of  alcoholic  excess  in  this  country  almost 
always  develop  before  the  age  of  thirty,  and  if  drinking  were  prohib- 
ited to  those  below  that  age,  there  would  be  but  little  trouble.  Wine 
drinking,  if  we  except  champagne  drinking,  is  almost  never  a  cause 
of  alcoholism  in  this  country,  and  is  a  much  less  important  factor  than 
beer.  This  is  largely,  no  doubt,  due  to  the  fact  that  wine  is  relatively 
little  drunk  in  America.  Beer  and  ale,  if  used  in  excess,  are  most  in- 
jurious forms  of  alcoholic  beverage,  except  to  out-door  workers,  be- 
cause they  lead  to  digestive  and  metabolic  disturbances.  It  would  be 
wise  to  forbid  the  use  of  alcohol  to  those  under  thirty,  except  in  the  form 
of  light  wines  or  beer,  and  those  only  to  workmen  and  people  who  live 
out  of  doors.  Even  after  this  age  it  should  only  be  given  to  the  certified 
immunes,  that  is,  to  those  able  to  drink  moderately. 

It  follows  that,  theoretically,  at  least,  the  sale  of  alcohohc  liquors 
should  be  controlled  by  the  Boards  of  Health. 

It  would  not  be  wise  to  abolish  the  use  of  alcohol  altogether  from 
civilization  until  we  can  be  sure  it  has  no  good  function,  or  until  we 
can  be  sure  that  its  abolition  would  not  be  followed  by  the  use  of  more 
injurious  substitutes.  It  is  impossible  to  deny  that  civilization  has 
satisfactorily  advanced,  despite  alcohol,  and  has  shown  its  finest  types 
among  those  nations  who  have  used  it  most.  Owing  to  the  fact  that 
sanitation  and  civihzation  have  developed  a  rather  more  delicate  type 
of  nervous  organization,  and  to  the  fact  that  sanitary  care  has  kept 
more  of  the  unstable  and  weakly  alive,  we  cannot  use  alcohol  as  freely 
as  formerly.  Therefore,  alcohol  has  got  to  be  used  more  and  more 
carefully,  and  under  closer  supervision  and  perhaps  finally  will  have  to 
be  abolished  absolutely  from  general  use. 

Arterial  sclerosis  is  a  condition  brought  about  by  many  of  the  factors 
that  have  been  here  enumerated  as  causing  nervous  disease.  Its  special 
and  direct  importance  will  be  shown  in  the  special  chapters. 

Reflex  Causes. — Among  other  causes  are  local  disease  of  viscera, 
such  as  renal,  uterine,  and  ovarian  diseases,  dyspeptic  and  liver  dis- 
orders, visual  and  auditory  troubles.  Reflex  irritations  are  distinc- 
tively exciting  causes,  but  with  few  exceptions  they  cannot  cause  a 
nervous  disease  unless  there  is  a  predisposition  to  it.  They  may,  how- 
ever, cause  many  distressing  nervous  symptoms,  such  as  pain,  spasm, 
and  even  convulsion. 


CHAPTER  III 

GENERAL  PATHOLOGY 

The  following  is  a  list  of  the  forms  of  disease  which  affect  the  nervous 
system : 

1.  Malformations;  incomplete  development,  or  agenesis;  defective 
development,  or  dysgenesis. 

2.  Hypersemia,  anaemia,  hemorrhage,  oedema,  and  arterial  and 
venous  diseases. 

3.  Degeneration  and  atrophy,  softening,  sclerosis,  classed  as  regres- 
sive processes. 

4.  Inflammations. 

5.  Tuberculosis  and  syphilis. 

6.  Tumors  and  parasites;  4,  5,  and  6  being  classed  as  progressive 
processes. 

7.  Nutritive  and  functional  disorders,  including  disorders  asso- 
ciated with  metabolic  and  glandular  defect,  such  as  acromegaly  and 
exophthalmic  goiter. 

The  pathology  of  most  of  the  above  types  of  morbid  processes  will 
be  given  elsewhere,  and  does  not  call  for  discussion  here. 

Degeneration  and  Sclerosis. — By  degeneration  is  meant  in  pathology 
a  gradual  death  of  the  nerve-cells  and  fibres,  or,  in  other  words,  of  the 
parenchyma  of  the  organ.  The  cells  swell  up,  become  granular  and 
fatty,  and  then  either  break  up  and  become  absorbed  or  enter  into  a 
condition  of  a  dead  coagulum  (coagulation  necrosis).  Degenerations 
may  be  acute  or  chronic,  primary  or  secondary. 

Acute  neural  degeneration  causes  a  condition  known  as  softening  or 
necrosis.  It  is  due  to  cutting  off  of  vascular  supply,  direct  injury,  and 
to  necrotic  and  inflammatory  poisons  attacking  the  neurons.  Acute 
degeneration  may  be  followed  by  a  reparative  process,  which  is  called  a 
reparative  or  reactive  inflammation,  and  which  ends,  perhaps,  in  produc- 
ing a  cicatrix  or  sclerosis. 

Chronic  degeneration  is  a  slow  neuronic  death  and  is  accompanied 
and  followed  by  a  proliferative  process  which  results  in  the  production 
of  connective  tissue  and  sclerosis  or  gliosis.  Degeneration  is  by  some 
writers  classed  as  a  degenerative  or  parenchymatous  inflammation. 

Sclerosis  is  a  process  of  connective-tissue  proliferation,  as  a  result  of 
which  the  normal  or  injured  parenchyma  is  supplanted  by  neuroglia 

28 


GENERAL    PATHOLOGY  29 

and  fibrous  tissue.  The  word  sclerosis  is  usually  employed  in  describ- 
ing degenerative  diseases,  though  it  indicates  the  result  rather  than  the 
primary  nature  of  the  process.  In  the  nervous  system  there  is  often 
an  increase  or  proliferation  of  neuroglia  tissue  in  the  processes  of  de- 
generation. Exactly  how  large  a  factor  this  is  cannot  yet  be  said.  In 
one  form  of  sclerosis^ — multiple  sclerosis — ^the  process  of  neuroglia  pro- 
liferation seems  to  be  the  primary  one,  nerve-cell  destruction  following. 
Hence  this  type  of  sclerosis  is  classed  with  the  proliferative  inflammatory 
processes. 

Degenerations  are  caused  by  certain  poisons,  such  as  arsenic,  phos- 
phorous, lead  and  the  poisons  of  infectious  disease.  Degenerations  also 
result  from  obliterating  arteritis,  such  as  occurs  in  old  age  or  from  humoral 
poisons.  Degenerations  sometimes  are  due  apparently  to  an  inherent 
defect  in  the  cell  nutrition — a  premature  death  of  it;  and  to  causes 
yet  unknown.  The  question  as  to  whether  certain  scleroses  are  forms  of 
productive  inflammation  or  of  chronic  degeneration  is  one  that  has  been 
much  debated  in  the  past.  It  is  quite  certain  now  that  most  of  the  so- 
called  chronic  inflammations  of  the  nervous  centres  are  really  degenera- 
tive processes,  and  that  the  primary  trouble  is  in  the  parenchyma,  and 
not  in  the  connective  tissue. 

Gliosis. — When  the  pathological  process  is  the  result  of  a  prolifera- 
tion of  neuroglia,  not  of  connective  tissue,  it  is  called  gliosis. 

Nutritive  and  Functional  Disorders. — Under  this  head  are  included 
defects  due  to  heredity,  to  disorders  of  the  blood  and  blood-glands,  to 
defects  in  metabolism,  to  poisons,  extrinsic  and  autochthonous,  and  to 
local  diseases. . 


CHAPTER  IV 
GENERAL  SYMPTOMS 

When  the  nervous  system  is  disordered  it  produces  various  symp- 
toms, which  are  classified  and  receive  names  according  to  the  parts 
affected  and  the  kind  of  change  present.  The  general  name  given  to 
any  kind  of  morbid  nervous  state  is  neurosis  and  the  general  name 
for  any  morbid  mental  state  is  psychosis.  When  the  neurosis  affects 
the  motor  sphere,  whether  in  the  brain  or  cord  or  nerves,  it  is  a  motor 
neurosis;  when  the  sensory  parts  are  disordered  we  have  a  sensory 
neurosis.  In  the  same  way  we  have  trophic,  thermic,  vasomotor  and 
secretory  neuroses. 

The  symptoms  of  nervous  disease  can  be  to  a  large  extent  divided 
in  accordance  with  the  kind  of  disturbances  present.  Now  a  function 
can  be  disordered  in  three  ways.  It  may  be  exaggerated,  lessened, 
to  the  point  perhaps  of  entire  loss  of  function,  or  it  may  be  perverted. 
In  order  to  indicate  this,  certain  Greek  prefixes  are  used.  They  are 
''hyper,"  which  means  excess;  "hypo,"  meaning  diminution;  ''a"  or 
"an,"  indicating  entire  loss;  and  ''para,"  meaning  perverted.  Thus  we 
have,  for  example,  hypersesthesia,  or  excessive  sensibility;  anaesthesia, 
or  loss  of  sensibility;  and  parsesthesia,  which  means  perverted  sensibility. 

Finally,  nervous  symptoms  are  often  spoken  of  as  objective  or  sub- 
jective. The  former  are  those  symptoms  which  can  be  seen  or  directly 
noted  by  the  physician  without  depending  on  the  patient's  statements. 
The  subjective  symptoms  are  those  which  are  felt  by  the  patient,  but 
give  no  outward  sign.  Thus  headache  is  a  subjective  symptom, 
paralysis  is  an  objective  one. 

So  far  we  have  been  grouping  together  only  like  kinds  of  symptoms; 
but  it  happens  that  one  nervous  disease  may  have  quite  different 
kinds,  some  being  motor,  some  trophic  or  sensory.  Thus  nervous  dis- 
eases practically  are  to  a  considerable  extent  classified  not  functionally 
but  anatomically ;  and  we  have  spinal  cord  and  brain  diseases,  gastric  and 
sexual  neuroses,  and  so  on. 

Nervous  sym'ptoms,  however,  are  always  grouped  together  in  accord- 
ance with  the  physiological  function  disturbed.  So  that  we  have  the 
following  tabulation  (see  also  Fig.  17) : 

1.  Mental  and  cerebral. 

2.  Motor  and  reflex. 

30 


GENERAL    SYMPTOMS  31 

3.  Sensory  (general,  and  special  sense  neuroses). 

4.  Trophic. 

5.  Vasomotor  (angioneuroses) . 

6.  Secretory  (secretory  neuroses). 

Combinations  of  these  groups  of  symptoms  may  affect  various 
organs.  They  are  called  mixed  neuroses.  Combinations  of  mental 
and  nervous  symptoms  form  psychoneuroses. 

The  particular  symptoms  which  nervous  diseases  cause  will  be 
described  and  recorded  under  the  several  heads  given  above. 

1.  The  mental  symptoms  include  all  those  found  in  insanity,  idiocy, 
and  imbecility,  and  will  not  be  given  in  detail  here.  The  common 
symptoms  met  with  by  the  neurologist  are  mental  irritability,  depression, 


r\/n  Psychoses 


inesioncuroses 
Aesthesioneuroscs 

Secretory  &iro£)}ii& 

VcLscmofor 

Fig.   17. — Diagram  illustrating  the  principle  of  the  classification  of  nervous  symp- 
toms, aside  from  special  sense  neuroses. 

emotional  excitement,  morbid  fears,  volitional  weakness  and  lack  of 
self-control,  persistent  or  fixed  ideas,  weakness  of  memory  and  of  power 
of  concentration,  and  a  tendency  to  hypnotic  and  somnambulistic  states. 

Certain  symptoms  due  to  disturbance  of  brain  function  are  called 
cerebral  or  cerebellar.  They  include  such  conditions  as  vertigo,  disorders 
of  equilibrium,  stereognosis,  aphasia,  cerebellar  ataxia,  and  many 
symptoms  connected  with  the  special  senses,  which  will  be  described  in 
the  special  chapters  later. 

2.  Motor  Symptoms. — The  symptoms  of  disordered  motility  are  as 
follows : 

(A)    Symptoms  of  exaggerated  or  perverted  motility. 

Tremor:   (a)   Fibrillary    and    wave-like    movements    of     muscles 
(myokymia) . 
(6)  Tremor  proper. 
Rhythmical  spasm,  athetosis. 
Convulsion. 

Myoclonia,  a  general  name  for  muscular  twitchings  and  including 
the  choreic  and  tic  spasms. 
Hypertonia  and  contracture. 


32  DISEASES    OF   THE    NERVOUS    SYSTEM 

Forced  and  associated  movements. 
Ataxia  and  asynergy. 
Exaggerated  reflex  conditions. 

(B)    Sympto7ns  of  lessened  motility. 

Paralysis  and  paresis,  myasthenia,  muscular  atrophy. 
Loss  of  reflexes,  superficial  and  deep. 
Hypotonia  or  lessened  muscular  tonus. 

The  particular  characteristics  of  these  different  symptoms  will 
be  best  shown  in  the  description  of  the  special  diseases,  but  a  brief 
account  will  be  given  here. 

Tremor  is  the  result  of  a  disorder  in  the  tonic  innervation  of  muscles, 
and  the  cerebello-mid-brain  mechanisms  are  important  factors  in  many 
types.  Muscles  are  kept  normally  in  a  state  of  slight  tension  with  rhyth- 
mical impulses  passing  down  at  the  rate  of  about  twelve  per  second. 
When  the  rhythm  and  force  of  these  normal  impulses  are  interfered  with 
we  have  tremor.  The  simplest  form  of  tremor  is  one  in  which  the  normal 
rhythmic  impulses  have  an  apparently  exaggerated  force.  This  causes  a 
fine  tremor  of  eight  to  twelve  vibrations  per  second  (Fig.  19) .  When  there 
is  an  interruption  to  some  of  the  impulses  we  have  a  coarse  tremor.  Here 
the  vibrations  are  four  to  eight  per  second  caused  by  a  partial  or  complete 
dropping  out  of  the  alternate  impulse.  Various  technical  names  are  used 
in  describing  the  tremors.  We  have  the  fine  and  coarse,  as  described 
Intention  tremor  is  one  that  occurs  on  voluntary  movement,  and  is 
opposite  in  kind  to  the  passive  tremor  or  tremor  of  rest,  which  does  not 
increase  on  voluntary  effort.  Tremor  is  sometimes  of  a  coarse,  jerky,  and 
inco-ordinate  character,  and  these  words  are  then  used  to  indicate  it. 

Fibrillary  tremor  or  myokymia  is  a  fine  twitching  of  the  individual 
strands  or  parts  of  muscles,  and  occurs  usually  when  they  are  wasting 
from  toxic  or  neurotrophic  influence.  Closely  related  to  it  are  the  wave- 
like contractions  of  the  muscle-body  without  motor  effect. 

Convulsions  consist  of  abnormal  and  exaggerated  muscular  con- 
tractions occurring  in  rapid  succession.  Convulsions  may  be  clonic, 
i.e.,  the  muscles  rapidly  and  alternately  contract  and  relax  in  an  ex- 
aggerated and  irregular  way;  or  they  may  be  tonic,  i.e.,  contracted 
suddenly  and  steadily  for  several  seconds  or  even  minutes.  When  a 
tonic  muscular  contraction  is  painful  it  is  called  cramp.  Convulsions 
may  be  co-ordinate.  In  this  case  the  patient  moves  the  limbs  and 
body  in  a  more  or  less  purposeful  way.  He  throws  himself  about  the 
bed,  jumps,  kicks,  strikes,  tears  the  clothes,  etc.  Convulsions  are 
usually  accompanied  with  loss  of  consciousness. 

Myoclonia  is  a  term  used  to  indicate  muscular  twitchings  of  various 
types,  such  as  those  of  chorea  and  the  "tics." 


GENERAL    SYMPTOMS 


33 


Choreic  rnovenients  are  sudden  jerking,  twitching  movements  of 
different  groups  of  muscles.  The  movements  are  purposeless  and 
are  not  under  control  of  the  will.  Convulsive  tic  is  a  form  of  spasmodic 
movement  confined  to  certain  groups  of  muscles  which  work  together 
for  a  common  purpose,  like  those  of  the  face,  or  eyes,  or  larynx.  The 
movements  in  the  "tics"  are  definite  in  character  and  are  limited  to 
muscles  physiologically  grouped  for  a  special  function.  Thus  we  have 
tics  of  the  muscles  of  expression,  or  of  respiration,  or  speech,  or  locomotion. 

OPTIC  TRACT  TECTUM  MESENCEPHALI 

1  RED  NUCLEUS 

JECTO-SPINAL  TRACT 
,      RUBRO-SPINAL  TRACT 


METATHAIAMUS 
THAIAMUS 


BRACHIUM  CONJUNCTIVUM 

,-  LEMNISCUS  MEOIALIS 


,V  LEMNISCUS  LATERALIS 
CEREBELLUM 


CORPUS  STRIATUM 
CEREBRAL  HEMISPHERE 


CEREBRO-SPINAL      ,  ^  , ,.    ., 
TRACT' '      X''-4 
OLTACTORY  NERVE 


Fig.  18. — Showing  in  detail  the  neuronic  architecture  of  the  nervous  sj^stem  in  the 
human  embryo.      (Cunningham.) 


Athetosis  is  a  name  given  by  Hammond  to  a  peculiar  form  of  move- 
ment characterized  by  slow,  successive  flexion,  extension,  pronation, 
and  supination  of  the  fingers  and  hand  and  arm,  or  of  analogous  move- 
ment of  the  toes  and  feet.  The  motion  rarely  ceases  in  waking  hours 
except  for  a  short  time.  The  contractions  are  forcible,  steady,  and 
even,  and  sometimes  painful.  The  hand  assumes  characteristic  posi- 
tions. 

A  contracture  is  a  tonic  muscular  contraction  of  long  duration,  i.e., 

3 


34 


DISEASES    OF    THE    NERVOUS    SYSTEM 


days  or  months.  A  contracture  may  be  functional  or  organic;  and  in 
order  to  test  this,  one  must  find  whether  it  ceases  during  sleep  or  under 
an  anaesthetic;  if  so,  it  is  functional  (see  Hysteria).  It  may  be  para- 
lytic; i.e.,  due  to  paralysis  of  opposing  muscles,  or  it  may  be  due  to  a 
continuous  spasm. 

In  forced  movements  the  patient  suddenly  and  involuntarily  is  thrown 
forward,  sideways  or  whirled  about  in  various  ways. 

Associated  movements  are  those  which  occur  involuntarily  in  a  limb 
or  muscle  at  rest  when  the  corresponding  limb  or  muscle  is  moved  on 
the  opposite  side.  Thus  in  hemiplegia  the  movement  of  the  normal 
arm  may  excite  a  movement  in  the  one  paralyzed.  The  patient  is  given 
a  piece  of  chalk  in  each  hand,  and  each  hand  is  placed  upon  a  black- 
board lying  on  the  table;  attempts  at  drawing  lines  with  the  sound  arm 
cause  movements  of  a  similar  kind,  but  less  perfect,  on  the  paralyzed 
side. 


A|l«.^|/%l^/A#/^i//*AAAUJi/|yiiiAA/WWw/l^l^^ 


Fig.  19.- 


-Diagram  of  a  fine  tremor.     Ten  of  the  divisions  on  the  lower  line 
equal  a  second. 


Myoidema  is  a  tonic  spasm  of  a  part  of  a  muscle.  It  is  produced 
by  a  sharp  blow  upon  the  muscle.  This  causes  the  muscular  fibers 
to  bunch  up  into  a  small  tumor  for  several  seconds.  Its  presence  may 
indicate  rapid  muscular  wasting  from  exhausting  disease,  or  a  toxic 
state. 

Idiopathic  muscular  spasm  is  a  phenomenon  of  a  similar  nature. 
When  the  belly  of  a  muscle  is  struck  with  a  dull  instrument,  a  welt  of 
contracted  muscle  appears  and  lasts  several  seconds.  It  indictes  an 
exaggerated  muscular  irritability. 


B.  Symptoms  of  Lessened  Motility 

Paralysis  or  akinesis  is  a  loss  of  motor  power.  Monoplegia  is  a 
condition  in  which  one  limb  is  paralyzed;  hemiplegia  one  in  which 
one-half  the  body  is  paralyzed;  and  paraplegia  one  in  which  the  two 
lower  limbs  are  affected.  Sometimes  a  double  hemiplegia  or  diplegia 
occurs.  The  term  paralysis  is  sometimes  used  to  indicate  loss  of  any  kind 
of  function,  as  paralysis  of  sensation  or  secretion. 

Paresis  is  a  term  used  to  indicate  a  partial  paralysis.     It  is   Hot 


GENERAL    SYMPTOMS 


35 


to  be  confouiulcd  with  the  term  general  paresis,  whicli  is  a  foiin  of 
insanity. 

The  Reflexes. — When  an  impulse,  started  in  an  afferent  nerve,  reaches 
the  spinal  cord  or  medulla  and  is  thence  reflected  upon  an  efferent  nerve, 
the  result  is  called  a  simple  reflex  action.  The  process  is  an  invol- 
untary one.  It  ordinarily  occupies  one-tenth  to  one-twelfth  of  a  sec- 
ond. The  afferent  nerve  may  be  an  ordinary  cutaneous  sensory  nerve, 
or  it  may  l)e  a  special  nerve  whose  function  is  to  excite  reflex  action. 
These  latter  nerves  are  called  excito-reflex.  This  kind  is  principally 
supplied  to  the  viscera. 

In  neurology  we  have  to  do  with  three  kinds  of  simple  reflexes: 

The  skin  or  superficial  reflexes. 

The  deep  reflexes. 


Fig.  20.— Babinski  reflex. 


The  visceral  reflexes. 

The  idiopathic  or  direct  muscle  response  is  not,  strictly  speaking,  a 
reflex. 

All  these  may  be  exaggerated,  modified,  lessened,  or  absent.  Further 
description  of  the  reflexes  will  be  given  under  the  head  of  diagnosis. 

The  simple  reflexes  are  combined  to  form  compound  or  higher  and 
more  complex  reflexes,  which  underlie  automatic  actions. 

3.  Sensory  Symptoms. — The  sensory  functions  include  all  those 
belonging  to  the  nerves  of  general  and  special  sensation.  Sensory 
nerves  have  a  part  in  reflex  action  and  in  the  inhibition  of  motor  and 
other  functions.  The  nerves  of  special  sense  when  deranged  show 
various  phenomena,  which  will  be  described  in  more  detail  later.  In 
general  there  may  be  depression  or  loss,  increase  or  perversion  of  their 
function.     In  accordance  with  this  we  have: 


36  DISEASES    OF    THE    NERVOUS    SYSTEM 

AncBsthesia,  which  is  a  loss  of  tactile  sensibility. 

Analgesia,  a  loss  of  sensibility  to  pain. 

Thermo-ancBsthesia,  a  loss  of  sensibility  to  temperature.  There 
may  be  loss  of  cold  sense,  of  heat  sense,  or,  as  is  usually  the  case, 
of  both  senses. 

The  term  anaesthesia  is  often  used  with  a  general  meaning  to  indi- 
cate loss  of  all  forms  of  sensibility.  Anaesthesia  in  this  sense  is  a  symp- 
tom referred  to  the  skin,  bones,  mucous  membranes,  special  senses  or 
viscera.  The  muscles  have  two  kinds  of  sensibility:  a  sensibility  to 
pain  and  pressure  and  a  special  muscle  sense.  Anaesthesia  of  the  pain- 
pressure  sense  of  muscle  is  called  loss  of  muscular  sensibility  or  muscular 
analgesia.  Anaesthesia  of  the  special  muscle  sense  is  one  of  the  factors 
in  causing  a  symptom  known  as  ataxia. 

Ataxia  is  a  symptom  due  to  loss  of  the  special  sensibility  of  the  mus- 
cle, articular  surfaces  and  tendons,  causing  irregular  and  inco-orclinated 
movements.  This  special  sense,  sometimes  called  deep  sensibility,  in- 
forms the  individual'  of  the  degree  and  strength  of  muscular  movements, 
and  by  it  definite  and  co-ordinated  movements  are  made  possible.  The 
weight  of  objects  and  position  of  the  limbs  are  also  determined  by  it. 
In  static  ataxia  there  is  loss  of  the  power  to  preserve  perfectly  the  equilib- 
rium when  standing.  In  locomotor  or  motor  ataxia  there  is  loss  of  power 
to  co-ordinate  the  limbs  properly  in  motion.  In  both  these  conditions 
there  is  also  usually  a  loss  of  power  to  appreciate  weights  or  the  position 
of  the  limbs. 

Cerebellar  ataxia  is  a  form  of  inco-ordination  and  disturbed  equilib- 
rium due  to  disease  of  the  central  organ  of  equilibration,  viz.,  the 
cerebellum.  Cerebellar  ataxia  is  due  to  disturance  of  (a)  the  equilibrium 
mechanism,  (6)  and  of  certain  co-ordinating  and  tonic  mechanisms  which 
enable  one  to  move  the  segments  of  the  body  in  proper  degree  and 
rhythm.  Their  disturbance  causes  symptoms  called  asynergy,  adio- 
kokinesis,  and  hypermetria.  These  will  be  described  later  in  connection 
with  the  diseases  of  the  cerebellum. 

Aster ecgnosis. — The  ability  to  recognize  the  form  of  objects  held 
in  the  hand  or  on  other  parts  of  the  body  is  called  stereognosis ,  and  its 
loss  aster eognosis.  It  is  a  perceptive  process,  due  to  the  fusing  and 
elaboration  of  cutaneous  and  deep  sensations,  especially  the  latter. 
Astereognosis  is  present  in  peripheral  or  spinal  lesions  where  there 
is  complete  tactile  anaesthesia,  and  where,  even  with  good  tactile  sense, 
there  is  loss  of  deep  sensibility.  As  complete  tactile  anaesthesia  is  rare 
in  cerebral  lesions,  the  cause  of  astereognosis  here  may  be  due  tp  injury 
of  the  center  for  deep  sensibility  or  of  perception  of  form.  The  lesion 
in  such  cases  is  localized  in  the  parietal  lobe. 

The  abihty  to  recognize  not  only  the  form   but  the  nature  of  an 


GENERAL    SYMPTOMS  37 

object  is  called  symbolia,  and  its  loss  asyniholia.  The  recognition  of 
the  nature  of  an  object  is  only  a  higher  elaboration  of  the  preceptive 
work  than  that  in  which  simply  form  is  recognized.  But  the  nature  and 
location  of  the  process  are  the  same,  practically,  as  for  stereognosis.^ 

Hyper (Esthesia  is  an  excessive  sensibility  to  touch,  contact,  and  other 
sensory  stimuli. 

Hyperalgesia  is  excessive  sensibility  to  pain,  and  is  nearly  identical 
with  tenderness. 

DyscBsthesia  is  simply  disagreeable  parsesthesia. 

ParcBsthesia  is  a  term  applied  to  all  the  morbid  general  sensations 
except  pain.  The  parsesthesias  include  such  feelings  as  numbness, 
prickling,  formication,  flushing,  burning,  itching,  coldness,  tickling, 
various  peculiar  visceral  sensations.  Ordinarily  in  speaking  of  par- 
sesthesise,  however,  we  refer  to  such  feelings  as  numbness,  prickling  and 
creeping. 

Delayed  sensation  is  a  symptom  in  which  an  appreciable  time  exists, 
usually  one  or  more  seconds,  between  the  time  of  applying  a  stimulus 
and  its  appreciation  in  consciousness.  Normally  a  tactile  sensation  can 
be  felt  and  responded  to  in  less  than  one-tenth  of  a  second. 

Transferred  or  referred  or  reflex  sensations  are  those  in  which  the 
irritation  is  made  at  one  point  and  felt  at  another.  Thus  an  irritation 
in  the  stomach  causes  a  pain  felt  in  the  forehead.  The  whole  class  of 
so-called  reflex  pains  are  really  transferred  sensations,  since  in  reality 
there  is  no  reflex  action  in  the  process,  as  will  be  seen  later.  Allochiria 
is  a  peculiar  form  of  transferred  sensation,  in  which  an  irritation  applied 
on  one  side  of  the  body  is  referred  to  a  corresponding  point  on  the  oppo- 
site side. 

4.  Trophic  Disorders. — These  consist,  so  far  as  relates  to  neurology, 
chiefly  of  hypertrophy  and  atrophy  of  nerves,  muscle,  cutaneous  and 
mucous  tissues,  joint  degenerations  and  various  skin  eruptions.  The 
trophoneuroses,  if  they  affect  joints,  are  called  arthropathies;  if  muscles, 
atrophies,  hypertrophies,  and  dystrophies;  or  if  with  atrophy  there  is  a 
great  substitution  of  fat,  the  condition  is  known  as  lipomatosis.  When 
nerves  are  affected  there  results  degeneration.  Trophoneuroses  of 
the  skin  produce  various  symptoms,  such  as  herpes,  pemphigus,  pig- 
mentation, leucoderma,  alopecia  and  bed-sores.  Trophoneuroses  so 
called  are  not  due  directly  to  lesions  of  trophic  nerves,  but  indirectly  to 
disturbance  of  vascular,  secretory,  sensory  and  motor  nerves.    • 

5.  Vasomotor  and  Secretory  Symptoms. — The  nerves  supplying  the 
blood-vessels  and  secreting  glands  work  together  and  are  usually  dis- 
ordered  together.     Separate   disturbances   of   the   vessels   and   glands, 

1  The  terms  tactile  amnesia  (Burr)  and  gnosia  and  agnosia  are  used  for  these  or  simi- 
lar perceptive  processes. 


38  DISEASES    OF    THE    NERVOUS    SYSTEM 

however,  occur.  Angioneurosis  is  the  term  given  to  disorders  of  the 
vasomotor  centre  and  nerves.  Angiospasm  is  a  condition  in  which 
there  is  increase  of  vasomotor  tone  and  spasmodic  contraction  of  the 
muscular  coats  of  the  arteries.  Angioparalysis  represents  the  opposite 
condition.  Such  disorders  affecting  the  skin  are  shown  by  pallor  and 
coolness  or  by  flushing  and  heat.  Angioataxia  is  a  condition  of  varia- 
bility and  irregularity  in  the  tonus  of  the  blood-vessels. 

The  secretory  neuroses  affect  the  functions  of  the  skin,  mucous 
membranes  and  special  glands.  Hyperidrosis  is  an  excessive  sweat- 
ing. Anidrosis  is  excessive  dryness.  Paridrosis  is  a  perversion  of 
secretion  in  which  peculiar  odors  or  colors  are  noted.  Hcemidrosis  is 
the  term  applied  to  bloody  sweating. 

The  secretions  of  the  internal  organs  are  controlled  by  nervous 
influences,  and  their  special  disturbances  often  form  part  of  the  symp- 
toms of  nervous  diseases.  Thus  we  have  watery  diarrhoea  in  Basedow's 
disease,  and  a  peculiar  membranous  discharge  from  the  bowel  in  asthenic 
states. 

The  glands  of  internal  secretion  and  particularly  the  thyroid  and 
pituitary  glands,  have  perversions  of  function  which  apparently  lead  to 
serious  nervous  symptoms,  which  will  be  described  under  the  head  of 
exophthalmic  goitre,  acromegaly,  and  dyspituitarism. 


CHAPTER  V 
DIAGNOSIS  AND  METHODS  OF  EXAMINATION 

The  diagnosis  of  a  nervous  disease  may  be  simply  a  clinical  one; 
that  is  to  say,  one  may  recognize  it  as  belonging  to  a  certain  known 
and  definite  group  of  symptoms.  Thus,  in  recognizing  the  phenomena 
of  epilepsy,  one  makes  a  clinical  diagnosis.  In  other  cases,  and  es- 
pecially in  all  organic  nervous  diseases,  the  physician  must  make  in 
addition  a  local  and  then  a  pathological  diagnosis.  That  is,  we  must 
determine  the  seat  and  nature  of  the  disease. 

A  diagnosis  is  made  by  first  getting  all  the  obtainable  facts  in  the 
patient's  past  history,  then  by  learning  from  him  all  his  subjective 
symptoms,  and  finally  by  making  an  examination  according  to  the 
technical  methods  to  be  here  described.  In  examining  a  patient,  it  is 
imperative  that  a  careful  search  for  diseases  outside  the  nervous  system 
first  be  undertaken.  Then  the  morbid  nervous  phenomena  should  be 
investigated.  The  physician  should  make  it  an  invariable  rule  to 
make  this  examination  in  a  certain  fixed  and  systematic  manner.  The 
best  method  is  first  to  get  the  family  and  personal  history,  and  then  to 
go  oyer  the  mental,  cerebral  and  special  nervous  functions  serially  in 
the  way  indicated  under  the  description  of  general  symptoms. 

In  addition  to  the  routine  methods  we  have  often  to  make  special 
tests  to  determine  the  existence  of  foreign  bodies,  fractures,  tumors 
and  disturbances  of  the  blood,  urine  and  cerebrospinal  fluids. 

In  investigating  the  family  history,  it  is  often  necessary  to  make 
very  direct  and  probing  inquiries,  for  patients  are,  as  a  rule,  inclined 
to  forget  or  ignore  the  existence  of  nervous  and  mental  disease  among 
relatives.  The  existence  of  consumption  and  inebriety,  epilepsy  and  sy- 
philis in  the  direct  line  are  very  important  facts;  so  also  are  those  con- 
cerning birth.  The  patient  should  be  questioned  closely  as  to  his 
previous  diseases,  especially  syphilis;  also  as  to  his  habits  in  relation 
to  sexual  indulgence,  indulgence  in  alcohol,  and  smoking.  In  women, 
the  tea  habit  should  be  inquired  into.  The  patient  may  be  allowed  to 
tell  his  own  story  first.  Proper  queries  should  be  put  to  supplement  this, 
and  finally  the  patient  should  be  asked  to  state  those  symptoms  which 
to  his  mind  are  main  and  dominant. 

We  will  now  go  over  the  above  points  in  detail. 

1.  The  Physiognomy,  complexion,  and  general  nutrition  are  first 
noted.      Many  nervous  disorders  are  compatible   with   a   very  healthy 

39 


40 


DISEASES    OF    THE    NERVOUS    SYSTEM 


appearance,  and  patients  often  make  the  introductory  apology,  "I 
don't  look  like  a  sick  person."  An  anxious  look,  restless  manner,  and 
excited  or  diffident  speech,  however,  often  show  something  wrong.  The 
nervous  trouble  is  usually  serious  in  reverse  proportion  to  the  voluble 
anxiety  of  the  patient  to  make  his  condition  exactly  understood.  The 
character  of  the  gait  may  reveal  at  once  the  nature  of  the  malady.  The 
dropped  foot  and  flaccid  swing  of  the  leg  in  poliomyelitis  and  neuritis, 
the  stiff  shuffling  march  of  paraplegia  from  myelitis,  the  waddling  move- 


FiG.  21. — Photograph  of  roof  of  the  mouth  of  a  drunkard  showing  torsus  palatinus. 

ments  of  juvenile  muscular  dystrophy,  and  the  bent  head  and  careful 
stamp  of  locomotor  ataxia  are  almost  of  themselves  diagnostic: 

Et  verus  incessu  patuit  morbus. 

The  speech  also  often  betrays  the  malady.  The  physician  soon  gets 
to  recognize  not  only  the  striking  symptoms  of  aphasia,  but  also  the 
weak  piping  of  paralysis  agitans,  the  stumbling  enunciation  of  paresis, 
and  the  peculiar  dysarthrias  of  multiple  sclerosis  and  bulbar  palsy.  As 
a  rule,  the  occurrence  of  speech  difficulties  in  adults  is  significant  of  organic 
and  often  serious  disease. 


DIAGNOSIS    AND    METHODS    OF    EXAMINATION  41 

In  the  chronic  and  constitutional  nervous  maladies  note  should  be 
made  of  the  marks  of  degeneration  or  the  neuropathic  constituent.  The 
nature  of  this  condition  has  already  been  described  under  the  head  of 
hereditary  causes  of  nervous  disease.  The  existence  of  degeneration  im- 
plies an  imperfect,  unusual,  or  unbalanced  development.  The  con- 
dition is  usually  shown  in  some  nervous  or  mental  peculiarity  or  defect 
in  the  individual,  and  degeneracy,  as  ordinarily  understood,  implies  a 
neuropathic  or  psychopathic  state.  But  degeneracy  may  also  mean  only 
a  lessened  vital  resistance  to  certain  forms  of  infection  or  injury,  as,  for 
example,  in  persons  of  a  tuberculous  tendency,  who  often  have  marks  of 
degeneracy.  These  marks  are  called  the  stigmata  of  degeneration. 
They  are  of  three  kinds:  anatomical,  physiological  and  mental. 

Anatomical  stigmala: 

Cranial  anomalies,  e.g.:  Asymmetrj^  of  cranium.  Microcephalus.  Peculiar 
shape  of  skull,  trigonal,  scaphocephalic,  plagiocephalic.  Facial  asymmetry  and  ex- 
cessive prognathism.     Large  jaws. 

Deformities  of  the  thorax,  such  as  the  pigeon-chest,  the  funnel-chest,  the  narrow 
barrel-shaped  chest  with  rib  set  too  obliquely  on  the  spine. 

Deformities  of  the  palate  and  uvula,  including  high  narrow  arch  and  the  torus 
palatinus. 

Anomalies  of  the  teeth,  tongue  and  lips. 

Anomalies  of  the  ej^-es:  narrow  palpebral  fissure,  muscular  insufficiency,  excessive 
astigmatism,  nystagmus. 

Anomalies  of  the  ears:  badly  placed,  ugly  shapes,  asymmetry,  adherent  or  lobeless 
ears,  markedly  conchoidal  ears. 

Anomalies  of  the  limbs,  genital  organs  and  bodj^  generally. 

Anomalies  of  the  skin,  excessive  hairiness  or  absence  of  hair. 

The  most  imporant  of  the  anatomical  stigmata  are  deviations  in 
the  symmetry  and  shape  of  the  skull,  defects  in  the  palate  and  under- 
jaws,  badly  shaped  ears,  badly  set  teeth,  badly  set  ribs  and  a  generally 
weak  and  badly  developed  body.  Stress  is  laid  upon  the  skull  because 
its  development  corresponds  with  that  of  the  brain.  The  palatal  stig- 
mata are  in  general  those  which  make  the  cavity  of  the  mouth  smaller, 
it  being  the  fact  that  the  mouth  cavity  increases  in  size  as  we  ascend  the 
vertebrate  series.  Abnormal  palates  are  found  in  about  10  per  cent,  of 
normal  people  (Charon)  and  in  from  46  to  80  per  cent,  of  abnormal. 
The  high,  narrow  palate  is  one  oftenest  seen  by  myself.  The  torus  pala- 
tinus or  longitudinal  ridge  on  the  hard  palate  is  significant  if  it  is  well 
marked  (Fig.  21).  The  importance  of  defective  ears  is  based  upon 
comparative  observations.  They  are  found  in  from  20  to  64  per  cent,  of 
more  or  less  abnormal  persons. 

While  many  of  the  stigmata  have  no  significance  in  themselves,  yet 
the  presence  of  a  number  of  them  is  of  great  importance,  for  neuroses 
or  psychoses  developed  among  this  class  have  a  much  more  unfavorable 


42  DISEASES    OF    THE    NERVOUS    SYSTEM 

prognosis.  It  is  especially  among  neurasthenics,  epileptics,  severe  forms 
of  hysteria  and  in  the  insanities  that  these  signs  are  to  be  looked  for  and 
studied.  Among  normal  men  about  two  or  three  anatomical  stigmata 
are  often  found;  among  lunatics,  criminals,  abortive  types  of  paranoia 
and  primary  forms  of  neurasthenia  the  number  is  much  greater. 

The  physiological  stigmata  include  tremor,  tics,  nystagmus  and 
hereditary  defects  in  the  muscular  system  leading  to  atrophies.  Ex- 
cessive or  defective  sensibility  of  the  cutaneous  and  special  senses,  de- 
fects in  speech,  perversions  of  the  sexual  and  other  instincts  are  to  be 
classed  here.  A  diminished  resistance  to  nervous  and  emotional  strain 
is  a  most  frequent  physiological  mark  of  neuropathy.  Allied  to  this  is 
the  excessive  sensibility  to  or  craving  for  the  action  of  tea,  coffee,  tobacco 
and  alcohol. 

The  mental  stigmata  include  all  those  factors  that  make  up  the 
erratic,  unbalanced  and  morbidly  emotional  individual.  The  specially 
morbid  note  in  these  persons  is  an  excessive  egotism,  an  intense  self- 
consciousness,  often  with  peculiar  disturbances  of  the  sense  of  personality. 
Mental  retardation  is  often  an  important  factor  in  the  examination  of 
a  nervous  patient.  This  is  especially  true  in  epilepsy  and  in  the  psycho- 
neuroses,  and  in  the  neuroses  of  childhood.  The  Binet-Simon  and 
certain  adult  tests  for  intelligence  are  to  be  employed  here. 

Physical  defects  due  to  disturbance  of  the  functions  of  the  glands  of 
inter7ial  secretion  may  need  investigation,  and  this  would  come  in  a 
measure  under  the  head  of  physiognomy,  and  nutrition. 

2.  Investigation  of  Symptoms  of  Disordered  Motility. — In  studying 
the  attitude,  expression,  gait  and  speech,  some  notion  of  the  condition 
of  the  motor  functions  has  been  obtained.  Special  disturbances  of  the 
various  parts  must  then  be  investigated. 

Paralysis.^TliQ  patient  is  made  to  move  the  arms,  legs,  trunk,  head, 
facial  muscles,  eyes  and  tongue,  etc.,  in  all  possible  ways.  If  paralysis  is 
found  the  degree  of  it  in  some  groups  of  muscles  can  be  measured  by 
dynamometers.  The  ordinary  hand  dynamometer  measures  the  degree 
of  paralysis  in  the  flexors.  The  average  power  of  pressure  on  the 
dynamometer  is,  for  an  adult,  40  to  50  kilograms  for  the  right  hand,  and 
3  to  5  kilograms  less  for  the  left.  A  woman  has  about  two-thirds  of  the 
power  of  a  man.  A  good  idea  of  the  degree  of  paralysis  can  be  got  by 
making  the  patient  take  the  physician's  two  hands  with  his  own  and 
squeeze  each  at  the  same  time.  A  malingerer  or  hysteric  will  often  in 
this  waj^  unconsciously  press  much  harder  than  he  is  aware.  The 
physician's  own  ingenuity  will  suggest  various  Avays  of  testing  the 
strength  of  the  leg  and  thigh  muscles,  such  as  making  the  patient  rise  on 
one  toe,  climb  upon  a  chair,  push  against  an  object  with  his  foot,  etc. 


DIAGNOSIS    AND    METHODS    OF    EXAMINATION 


43 


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44  DISEASES    OF    THE    NEKVOUS    SYSTEM 

Some  paralysis  being  discovered,  we  try  to  determine  its  degree  and 
type.     Paralyses  are  of  four  types: 

1.  An  upper  neuron  type,  in  which  the  lesion  involves  the  cerebro- 
spinal motor  neurons.  The  paralysis  is  then  as  a  rule  hemiplegic,  and 
accompanied  with  spasticity  and  exaggerated  deep  and  lessened  skin 
reflexes;  it  is  not  accompanied  with  atrophy  of  the  muscles,  involved  or 
with  degenerative  electrical  changes. 

2.  A  lower  neuron  type,  in  which  the  lesion  involves  the  anterior 
cornual  cells  or  anterior  roots  of  the  spinal  cord,  or  the  corresponding  parts 
of  the  brain  stem  (pons-medulla).  The  paralysis  is  localized  in  the 
muscles  supplied  by  the  injured  neurons;  it  is  flaccid  and  associated 
with  atrophy  and  the  electrical  reactions  of  degeneration. 

3.  A  neural,  or  mixed  nerve  type  of  paralysis,  in  which  the  symptoms 
are  like  those  of  a  lower  neuron  type  plus  sensory  symptoms,  such  as  pain 
and  anaesthesia. 

4.  A  psychic  type  of  paralysis,  in  which  the  paralysis  depends  upon 
a  mental  state.  Here  the  paralysis  may  be  hemiplegic,  paraplegic  or 
monoplegic  but  it  is  not  accompanied  with  spasticity,  or  atrophy,  and 
it  is  generally  accompanied  with  anaesthesia. 

Tremor  is  usually  most  noticeable  in  the  hands  and  is  tested  by 
making  the  patient  hold  out  the  hands  and  arms  at  full  length,  spreading 
out  the  fingers  at  the  same  time.  To  determine  whether  the  tremor  in- 
creases on  volitional  movement,  give  the  patient  a  full  glass  of  water, 
let  him  hold  it  out  for  a  moment,  then  bring  it  to  his  mouth  slowly.  If 
the  tremor  increases  with  this  movement  it  is  called  "intentional."  As  a 
general  rule,  the  tremor  of  organic  disease  is  coarse  in  type  and  increased 
by  volitional  movement,  and  ceases  during  rest  of  the  extremity.  Func- 
tional tremors  are  usually  fine  in  type  and  continuous,  except  on  complete 
rest  and  relaxation.  In  most  forms  of  tremor  the  hand  and  arm  shake  as 
a  whole.  In  other  forms  the  tremor  involves  only  the  fingers  or  hand  or 
forearm  and  hand.  Such  tremor  is  called  segmental.  It  is  especially 
seen  in  paralysis  agitans.  As  I  have  already  said,  tremor  may  be  fine  or 
coarse,  i.e.,  four  to  six  or  eight  to  twelve  per  second.  To  determine  this 
accurately  a  special  apparatus  is  needed;  but  one  can  with  a  little  expe- 
rience determine  this  fairly  well  by  observation  alone. 

While  coarse  tremor  as  stated  is  usually  a  sign  of  organic  disease  or 
of  paralysis  agitans,  it  occurs  also  in  hysteria  and  grave  conditions  of 
alcoholism.  Tremor  that  is  hardly  observable  by  the  eye  can  be  felt  by 
placing  one's  hand  against  the  extended  fingers  of  the  patient. 

Tremor  of  the  tongue  and  lips  and  facial  muscles  must  be  carefully 
looked  for.  It  is  tested  by  making  the  patient  close  the  eyes  tightly  and 
show  the  teeth  or  protrude  the  tongue.  Facial  tremor  if  very  marked 
usually  indicates  a  serious  condition  of  nervous  exhaustion,  alcoholic 


DIAGNOSIS    AND    METHODS    OF    EXAMINATION  45 

poison,  or  some  other  toxaemia  or  paresis.  Tremor  of  the  whole  head  due 
to  the  neck  muscles  must  be  distinguished  from  secondary  shaking  of  the 
head  due  to  a  tremor  of  the  trunk. 

Finally,  it  is  to  be  remembered  that  tremor  is  a  rhythmical  disturb- 
ance and  it  should  be  distinguished  from  the  jerky  irregular  ataxic  move- 
ments of  cerebellar-mid-brain  disease.  These  always  cease  entirely  when 
the  patient  is  lying  on  his  back  and  making  no  movements. 

Nystagmus  is  a  form  of  tremor  indicating  cerebellar  or  mid-brain 
disturbance. 

Choreic  movements,  tics,  associated  and  forced  movements,  and  con- 
vulsions are  the  expression  of  certain  diseases  and  are  described  elsewhere. 

The  Examination  of  the  Reflexes. — These  are  of  three  kinds:  (1) 
the  superficial  or  skin,  (2)  the  deep,  (3j  the  visceral. 

1.  A  skin  or  superficial  reflex  is  produced  by  scratching,  pinching 
or  irritating  the  skin.  The  result  is  a  contraction  of  the  muscles  supply- 
ing the  parts  near  or  under  the  irritation.  The  skin  reflexes  which  can 
be  ordinarily  brought  out  are  the  anal,  bulbo-cavernous,  plantar,  cre- 
masteric, epigastric,  abdominal,  scapular,  palmar,  and  certain  cranial 
reflexes. 

The  anal  reflex  is  brought  out  by  scratching  the  perineum.  It 
causes  a  contraction  of  the  sphincter  ani. 

The  bulbo-cavernous  reflex  is  brought  out  by  placing  a  finger  on  the 
urethra  just  back  of  the  scrotum,  and  pinching  or  pricking  the  glans  penis. 
This  causes  a  contraction  of  the  bulbo-cavernous  muscle. 

The  plantar  reflex  is  produced  by  tickling  or  scratching  the  soles  of 
the  feet.  This  causes  usually,  when  carefully  done,  a  slight  flexion  of 
the  toes.  In  many  cases  there  is,  however,  no  response.  In  irritable 
persons  and  children  there  is  a  sudden  dorsal  flexion  of  the  foot,  and  often 
a  contraction  of  the  inner  hamstring  muscles.  In  pathological  condi- 
tions involving  the  pyramidal  tracts  of  the  cord  and  the  motor  centres 
and  tracts  in  the  brain  there  is  a  dorsal  extension  of  the  great  toe,  some- 
times accompanied  with  a  fan-like  spreading  out  of  the  other  toes.  This 
is  called  the  Babinski  reflex  (Fig.  20).  A  similar  phenomenon  is  pro- 
duced by  firmly  compressing  the  muscles  of  the  calf  (Gordon  reflex) ,  and 
by  causing  the  patient  to  draw  his  leg  up  sharply  flexing  the  thigh  on 
the  abdomen  and  the  leg  on  the  thigh  (Strumpell  reflex) ;  or  by  pressing 
and  drawing  a  blunt  instrument  or  the  finger  sharply  down  along  the 
inner  side  of  the  tibia  (Oppenheim  reflex)  or  by  scratching  the  leg  behind 
the  external  malleolus  (Chaddock  reflex). 

The  cremasteric  reflex  is  brought  out  by  scratching  the  inner  side  of 
the  thigh  or  the  skin  over  Scarpa's  triangle.  It  causes  a  drawing  up  of 
the  testicle,  not  of  the  scrotum  alone,  on  the  same  side. 

The  abdominal  reflex  consists  of  a  contraction  of  the  abdominal  recti 


46 


DISEASES    OF    THE    NERVOUS    SYSTEM 


muscles,   caused  by  irritating  the  skin  over  the  outer  border  of  the 
rectus. 

The  epigastric  reflex  consists  of  a  contraction  of  the  upper  fibres  of 
the  rectus,  caused  by  irritating  the  sldn  of  the  same  region  higher  up. 

The  scapular  reflex  consists  of  a  contraction  of  scapular  muscles, 
caused  by  irritating  the  skin  over  them. 

The  palmar  reflex  is  produced  by  irritating  the  palms  of  the  hands. 
It  is  obtained  only  in  infants  and  the  reaction  is  flexion. 

The  cranial  reflexes  are  the  corneal  and  conjunctival,  a  reflex  contrac- 
tion of  the  lids  caused  by  lightly  touching  the  cornea  or  conjunctiva  with 
a  bit  of  cotton  or  a  camel's-hair  brush;  the  pupillary -skin  reflex,  which 
consists  of  a  dilatation  of  the  pupil  caused  by  scratching  the  skin  of  the 
cheek  and  chin;  the  supra-orhital  reflex  caused  by  striking  a  slight  blow 
over  the  supra-orbital  foramen;  the  naso-mental  reflex,  in  which  a 
contraction  of  the  levator  mentis  is  caused  by  a  tap  on  the  side  of  the 
nose. 

Skin  or  Superficial  Reflexes 


Superficial  Reflexes 

Method  of  Exciting 

Effect 

Localization 

1.  The         Supra- 

A tap  over  the  supra- 

Orbicularis contracts 

V-Vll 

orbital. 

orbital  foramen 

2.  Conjunctival  re- 

Touching   cornea,  or 

Orbicularis  contracts 

V-Vll 

flex. 

conjunctiva 

3.   Naso-mental.. .  . 

Blow  on  side  of  nose 

Levator    menti    con- 
tracts 

V-Vll 

4.  Palatal 

Touching  palate 

Palate  contracts 

IX-X 

5.  Pharyngeal 

Touching      posterior 
wall  of  pharynx 

Pharynx  contracts 

IX 

6.  Skin-pupillary . . 

Pinching  cheek 

Pupil  dilates 

V-cervical    sym- 
pathetic 

7.  Scapular 

Stimulation     of     the 

Movement        of 

C5-D1 

skin  over  the  scapula 

shoulder-blade 

8.  Palmar 

Irritation  of  the  palm 

Flexion  of  fingers 

C8-D1 

9.  Epigastric 

Stroking  from  nipple 

Drawing    in    of    epi- 

D7-D9 

downward 

gastrium 

10.  Abdominal 

Stroking  side  of  the 

Drawing    in    of    ab- 

D9-D12 

abdomen 

dominal  wall 

11.  Cremasteric. .  .  . 

Stroking      the      ad- 
ductor region  of  the 
thigh 

Elevation  of  testis 

L1-L2 

12.  Plantar  reflex. .  . 

Stroking  the  sole 

Dorsal  or    plantar 
flexion  of  toes 

S1-S2 

13.  Bulbo  -  caverno - 

Pinching    dorsum    of 

Bulbous  urethra  con- 

S3-S4 

sus. 

glans  penis 

tracts 

14.  Anal  reflex 

Pricking     the     peri- 

Contraction of  sphinc- 

S5 

neum 

ter  ani  externus 

DIAGNOSIS    AND    METHODS    OF    EXAMINATION 


47 


There  are  also  palatal  and  pharyngeal  reflexes.  The  superficial 
reflexes  depend  upon  the  integrity  of  the  reflex  spinal  arc,  and  to  a  less 
extent  upon  the  degree  of  cerebral  influence.  When  present,  they  show 
that  the  spinal  cord  at  the  level  through  which  the  impulses  travel  is 
healthy.  When  absent,  they  do  not  necessarily  indicate  much  of  any- 
thing, for  they  vary  in  amount  in  different  persons  and  at  different  ages 
being  always  more  active  in  the  young.  In  cerebral  hemiplegia  during 
and  after  the  acute  attack  the  abdominal  reflexes  are  absent  on  the 
affected  side.  This  reflex  is  also  often 
absent  in  multiple  sclerosis.  The 
supra-orbital  reflex  is  often  absent  in 
profound  hemiplegia  with  coma. 

The  deep  reflexes  are  sometimes 
called  tendon  reflexes,  though  this'  is 
not  a  strictly  correct  name,  since  they 
can  be  called  out  by  striking  perios- 
teum or  muscle  as  well  as  tendons. 
The  deep  reflex  in  all  these  cases  is 
not  a  true  spinal  reflex,  but  is  due  to 
the  direct  effect  of  the  concussion  or 
the  sudden  stretching  upon  the  muscle 
itself  which  is  in  a  condition  of  slight 
tonus.  Those  who  accept  this  view 
speak  of  the  deep  reflex  as  indicating 
the  myotatic  irritability  or  muscular 
tonus.  The  deep  reflex  implies  also 
the  integrity  of  a  reflex  arc. 

The  important  deep  reflexes  are  the 
patella-tendon  reflex  or  knee-jerk;  the 
ankle  reflex  or  ankle-jerk;  the  biceps, 
supinator,  pronator  and  triceps  reflexes ; 
the  scapulo-humeral  reflex;  the  jaw 
reflex  or  chin-jerk;  the  light  (or  pupil- 
lary) and  so-called  accommodation  (or  ciliary)  reflexes;  the  oculo-car- 
diac  reflex.     These  are  all  present  in  health  except  the  jaw-jerk. 

The  reflexes  are  of  diagnostic  importance,  for  they  are  absent  in  some 
diseases,  exaggerated  in  others,  and  in  certain  conditions  new  reflexes 
appear.  These  abnormal  reflexes  are  the  Babinski  reflex,  the  Hoffman 
reflex,  ankle  clonus  and  certain  pupillary  reflexes. 

The  patella  reflex  or  knee-jerk  consists  of  a  sudden  contraction  of 
the  quadriceps  femoris,  vastus  internus,  and  subcrureus  caused  by 
striking  the  patella  tendon  when  the  leg  hangs  loosely  at  right  angles 
with  the  thigh.     This  reflex  may  also  often  be  produced  by  striking 


Fig.  22. — Getting  the  knee-jerk. 


48 


DISEASES    OF    THE    NERVOUS    SYSTEM 


the  lower  part  of  the  muscle  itself.  The  activity  of  this  reflex  is  Id- 
creased  if,  at  the  same  time  that  the  blow  is  struck,  a  voluntary  con- 
traction of  some  other  muscles  is  made  by  the  patient.  Usually  the 
patient  is  told  to  pull  on  his  clasped  fingers  or  tightly  shut  the  hands. 
This  process  is  called  the  re-enforcement  of  the  knee-jerk  (see  Fig.  22). 
Such  re-enforcement  can  be  caused  by  irritating  the  skin  and  by  various 
sensory  or  psychic  stimuli.  The  nerve-roots  involved  are  those,  in 
man,  of  the  second  and  third  lumbar  segments.  The  peripheral  nerve 
is  the  anterior  crural.     The  essential  muscle  is  the  vastus  internus. 

The  biceps  reflex,  a  supinator  reflex,  and  a  pronator  reflex  are  said 
by  Babinski  to  be  always  present  in  normal  persons.  The  first  two  are 
obtained  by  striking  the  lower  tendon  of  the  partly  flexed  biceps  and  the 
lower  third  of  the  supinator  longus;  the  pronator  reflex  is  obtained 
by  striking  the  lower  head  of  the  ulnar  bone.  The  triceps  reflex  or 
elbow-jerk  is  brought  out  by  striking  the  triceps  tendon  while  the  arm 
is  supported  and  the  forearm  allowed  to  hang  down  loosely  at  right  angles 
to  the  arm.     These  reflexes  occur  in  normal  individuals. 

Deep  Reflexes 


Tendon,  Bone  or  Deep 
Reflexes 

Method  of  Exciting 

Effect 

Localization 

1.  Pupillary 

Expose  to  light;  and 

Pupil    responds  to 

1-111  ciliary  gan- 

reflexes 

test  accommodation 

to    light,    and 

glion 

accommodation 

Pons 

2.  Jaw  reflex 

Tapping    lower    jaw 
which  is  relaxed  half 
open 

Jaw  closes 

V 

3.  Biceps 

Tapping        biceps 
tendon 

Biceps  contracts 

C5-C6 

4.  Supinator  longus 

Tapping  styloid  pro- 

Supinator longus  con- 

C5-C6 

cess  of  radius 

tracts 

5.  Scapulo- 

Tapping      vertebral 

Teres    minor,    infra- 

C5-C6 

humeral 

border     of     scapula 

spinatus,   etc.,   con- 

near base 

tract 

6.  Pronator 

Tapping      head       of 
ulnar 

Pronation 

C6-C8 

7.  Triceps 

Tapping            triceps 
tendon 

Triceps  contracts 

C7-Thl 

8.  Carpo- 

Tapping   wrist 

Fingers  flex 

C8-Thl 

metacarpal 

9.  Knee 

Tapping          patellar 

Vastus  internus,  etc.. 

L3-L4 

tendon 

contract 

10.  Ankle 

Tapping            tendo- 
Achillis 

Calf  muscles  contract 

S1-S2 

The  jaw  reflex  or  jaw-jerk  is  brought  out  by  having  the  patient  open 
the  mouth  and  leave  the  jaw  relaxed.     A  flat  instrument  Hke  a  paper- 


DIAGNOSIS    AND    METHODS    OF    EXAMINATION 


49 


cutter  is  then  laid  on  the  teeth  of  the  lower  jaw,  and  if  this  is  struck 
smartly  the  elevators  of  the  jaw  contract.  The  light  reflex  is  tested  bj^ 
throwing  a  bright  light  into  the  eye;  and  the  ciliary  or  accommodation 
response  by  making  the  patient  look  at  a  distant  and  then  at  a  near 
object.  The  pupil  normally  dilates  in  the  former  case  and  contracts 
in  the  latter.  When  the  light  reflex  is  lost  while  the  accommodation 
action  remains,  the  condition  is  called  the  Argyll-Rohertson  pupil. 

The  reflex  path  is  probably  through  the  optic  nerve,  the  primary  optic 
centers,  third  nerve,  ciliary  ganglion  and  ciliary  nerves. 

The  oculo-cardiac  reflex  is  produced  by  pressing  firmly  on  the  ball  of 
one  or  both  eyes.  This  causes  a  slowing  of  the  heart  beat.  The  reflex  is 
usually  absent  in  locomotor  ataxia. 


Fig.  23. — Testing  pupillarj^  reflexes,  before  an  open  window. 

The  Hoffman  reflex. — ^A  sharp  snap  of  the  last  phalanx  of  the  middle 
finger  causes  flexion  of  the  index  and  thumb.  Its  presence  generally 
indicates  a  pyramidal  tract  lesion. 

Ankle  clonus  is  caused  by  having  the  seated  patient  extend  the  limb 
and  hold  it  rather  firmly  in  a  semiflexed  condition.  The  physician  takes 
the  foot  by  the  toe  and  heel  and  quickly  flexes  the  foot  on  the  leg.  He 
thus  suddenly  stretches  the  calf  muscles,  and  they  undergo  rhythmical 
contraction.  This  phenomenon  does  not  occur  in  healthy  people.  It  is 
found  in  involvement  of  the  cortico-spinal  tracts  and  it  usually  indicates 
organic  disease  of  the  cord.  A  pseudo-clonus  sometimes  occurs  in  which 
there  are  a  few  rhythmical  contractions  on  sudden  dorsal  flexion  of  the 
foot,  but  the  contractions  soon  subside.  This  is  seen  in  exhaustion  and 
toxic  states  and  in  hysteria. 

The  deep  reflexes  may  be  decreased,  delayed,  absent,  or  exaggerated. 
Their  exaggeration  is  common  and  not  of  special  clinical  significance. 


50 


DISEASES    OF    THE    NEKVOUS    SYSTEM 


The  absence  of  the  knee-jerk  or  ankle-jerk  is  of  great  significance,  indi- 
cating in  persons  who  have  no  paralysis  of  the  muscles,  locomotor  ataxia, 
nem-itis  or  some  toxaemia,  such  as  follows  diphtheria  or  exists  in  diabetes. 
The  Electrical  Conditions  in  Disturbances  of  Motility. — These  can- 
not be  understood  without  some  description  of  the  methods  of  using 
electricity,  and  hence  the  technic  of  electrical  examinations  for  purposes 
of  diagnosis  will  be  described  under  the  head  of  treatment. 

Examination  of  the  Disorders  of  Sensation. — The  object  of  examining 
the  sensory  functions  is  to  see  if  they  are  exaggerated,  perverted,  delayed  or 
lost,  and  to  locate  the  extent  of  the  disturbance.  Patients  differ  greatly 
in  their  intelligence  and  power  of  description,  so  that  great  care  must  be 

taken  in  drawing  conclusions  as  to 
sensory  disturbances.  In  examin- 
ing the  skin  and  muscle-senses,  the 
patient's  eyes  should  be  closed  and 
he  should  be  carefully  told  to  answer 
promptly  whenever  he  feels  the 
stimulus.  It  is  best  to  insist  that 
he  always  reply  in  the  same  way, 
e.g.,  using  the  word  ''now"  the 
moment  the  sensation  is  felt.  Many 
ingenious  instruments  have  been  de- 
vised, and  I  have  described  some  of 
them,  but  for  ordinary  purposes  a 
camel's-hair  pencil  or  a  bit  of  cotton 
wool  and  a  pin  answer  very  well. 

Loss  of  cutaneous  and  deep  sen- 
sibility produces  anaesthesias  and 
these  anaesthesias  like  paralyses 
have  different  characters  in  accord- 
ance with  the  series  of  neurons  in- 
volved. 

Anaesthesias,  cutaneous  and  deep,  may  like  paralyses  be  of  different 
types  in  accordance  with  the  part  involved. 

1.  Upper  neuron  anaesthesias.  If  the  upper  sensory  neiu'ons  of  the 
cerebrum  are  affected  the  anaesthesia  is  never  abslutely  complete,  and 
it  is  associated  usuallj^  with  a  hemiplegia. 

2.  Middle  neuron  anaesthesias.  If  a  lesion  lies  in  sensory  neurons 
of  the  cord  or  brain-stem  the  anaesthesia  may  be  of  a  dissociated  type; 
i.e.,  there  may  be  an  anaesthesia  to  pain  and  temperature,  but  not  to 
touch.  ■ 

3.  Peripheral  neuron  anaesthesias  may  be  complete,  or  have  various  de- 
grees of  completeness,  but  they  are  not  dissociated.     Protopathic  and 


Fig.  24. — Testing  for  ankle-jerk. 


DIAGNOSIS    AND    METHODS    OF    EXAMINATION 


51 


epicritic  variations  of  cutaneous  anaesthesia  are  all  due  to  lower  neuron  and 
peripheral  nerve  involvement. 

4.  Psychic  anaesthesias  are  rarely  absolute.  They  involve  the  entire 
half  of  the  body,  or  the  entire  body  or  one  limb,  and  affect  the  special 
senses  in  a  definite  manner  (see  hysteria). 

The  cutaneous  sensations  are:  (1)  The  tactile  sense,  which  includes 
pressure  and  contact;  (2)  the  temperature  sense,  which  includes  the 
heat  sense  and  cold  sense;  (3)  the  pain  sense.  The  first  two  are  special 
senses,  the  last  is  a  general  sense. 

To  test  the  tactile  sense,  blindfold  the  patient  and  use  the  aesthe- 
siometer.     This  is  an  instrument  with  two  rather  blunt  points,  which 


Fig.  25. — Bringing  out  ankle  clonus. 

can  be  separated  or  approximated.  A  hairpin  or  two  ordinary  pins 
can  be  used  in  its  stead.  Its  use  depends  upon  the  fact  that  the  power 
to  appreciate  the  contact  of  two  points  on  the  skin  gradually  approxi- 
mated varies  with  the  tactile  sensibility  of  the  patient.  The  tongue, 
finger  tips  and  lips  are  the  most  sensitive  points.  The  back,  arms  and 
thighs  the  least  sensitive. 

The  following  table  shows  the  average  distance  at  which  two  points 
are  appreciated  as  such  by  an  intelligent  adult : 

Tip  of  Tongue 1  mm.  (V^s  in.).  Tip  of  toes,  cheeks,  eyelids ...  12  mm. 

Tip  of  fingers 2  mm.                     Temple 13  mm. 

Lips 3  mm.                     Back  of  hands 30  mm. 

Dorsal  surface  of  fingers.  .  .   6  mm.                     Neck 35  mm. 

Tip  of  nose 8  mm.  Foi-earm,  leg,  back  of  foot. ...  40  mm. 

Forearm 9  mm.  Back .  .60-80  mm. 

Arm  and  thigh 80  mm . 

The  figures  vary  somewhat  with  the  thickness  or  softness  of  the 


52  DISEASES    OF    THE    NERVOUS    SYSTEM 

skin  and  with  the  dullness  or  keenness  of  the  nervous  organization.  If 
the  distances  are  double  those  given  above,  it  may  be  considered  in 
most  cases  abnormal. 

The  sense  of  contact,  which  is  a  form  of  tactile  sense,  is  tested  by 
touching  the  skin  very  lightly  with  a  hair  or  hair  brush  or  bit  of  cotton. 
The  sense  of  locality  or  power  to  localize  a  point  on  the  skin  that  has 
been  touched  varies  with  the  tactile  sense  and  with  the  muscular  sense. 
It  is  tested  by  placing  the  finger  lightly  on  a  given  spot  and  telling  the 
patient  with  closed  eyes  to  place  his  finger  on  the  part  touched.  He 
should  come  within  5  cm.  In  slight  degrees  of  anaesthesia  dependent 
upon  disease  of  the  sensori-motor  areas  of  the  cortex  of  the  brain  this 
is  an  important  test.  Further  tests  may  be  made  by  moving  points 
along  the  skin  and  taking  the  patient  to  indicate  the  direction  of  the 
motion. 

To  test  the  pressure  sense,  one  may  use  the  barsesthesiometer,  an 
instrument  made  with  a  spring  scale  measuring  the  amount  of  pres- 
sure made.  A  simpler  way  is  to  have  the  patient  rest  the  hands  on  a 
table  and  then  try  and  determine  the  weight  of  different  objects.  The 
lightest  weight  that  can  be  appreciated  on  the  hands  or  face  is  one  of 
about  0.02  gram  (gr.  ^i).  Differences  of  light  weights  of  1  and  5  grams 
and  of  25  and  30  grams  are  about  all  that  can  be  ordinarily  appreciated 
by  the  skin.  Much  smaller  differences,  of  0.5  to  2  grams,  can  be  detected 
if  great  care  is  used.  Weighted  rubber  balls  may  be  used  in  the  fore- 
going test.  I  prefer  to  use  differently  weighted  metal  bodies  held  by  a 
wire.  Pressure  sense  is  acute  on  the  forearm  and  abdomen,  where 
locality  sense  is  feeble;  also  on  the  brow,  temples  and  back  of  the  hand. 
By  the  use  of  these  tests  held  freely  in  the  hand  we  test  also  the  musculo- 
articular  or  deep  sensibility. 

The  tem'perature  sense  is  tested  by  test-tubes  filled  with  hot  and 
cold  water,  or  by  using  hot  and  cold  spoons,  or  roughly  by  breathing 
and  then  blowing  on  the  part.  A  thermo-aesthesiometer  may  be  used. 
This  has  a  round,  flat  surface  1  cm.  in  diameter,  and  contains  in  its 
terminals  thermometers  by  which  the  degree  and  differences  in 
temperature  may  be  noted.  A  small  heated  or  chilled  surface  is  appre- 
ciated much  less  easily  than  a  large  one. 

The  indifferent  range  where  objects  are  felt  to  be  neither  warm 
nor  cold  is  from  27°  to  30°C.  (80.6°  to  86°F.).  Fine  differences  (0.2° 
to  1.5°C.)  are  appreciated  above  the  indifferent  range.  Lower  down 
in  the  scale,  differences  from  1°  to  1.3°C.  (2°  to  3°F.)  are  appreciable. 
It  may  be  considered  a  morbid  symptom  if  temperatures  of  60°  to  65°F. 
are  not  felt  as  cold,  or  temperatures  of  86°  to  95°F,  are  not  felt  as  warm; 
also  ff  between  the  ranges  of  1°C.  (32°F.)  and  40°C.  (104°F.)  differences 
of  2°C.  are  not  appreciated.     A  painful  degree  of  sensitivenessto  heat 


DIAGNOSIS    AND    METHODS    OF    EXAMINATION 


53 


Fig.  26. — Showing  the  segmental  or  root  distribution  of  cutaneous  sensory  nerves 
on  the  right  side,  and  the  peripheral  distribution  on  the  left  side.  (Drawn  by  H.  T.. 
Shannon.) 


54 


DISEASES    OF    THE    NERVOUS    SYSTEM 


Fig.  27. — Showing  the  segmental  or  root  distribution  of  cutaneous  sensory  nerves 
on  the  left  side,  and  the  peripheral  distribution  on  the  right  side.  (Drawn  by  H.  T. 
Shannon.) 


DIAGNOSIS    AND    METHODS    OF    EXAMINATION  00 

or  cold  sometimes  exists.  These  conditions  are  called  hyperthermalgesia 
and  hypercyalgesia  (Skinner,  Starr).  When  the  heat  or  cold  is  intense, 
a  sensation  of  pain  is  felt.  Cold  pain  is  produced  more  easily  in  some 
places,  such  as  the  elbow,  than  in  others,  as  for  example,  in  the  finger  tips. 
Cold  pain  is  produced  by  temperatures  of  from  +  2.8°C.  to— 11.4^C. 
Heat  pain  is  produced  by  temperatures  of  from  36.3°C.  to  52.6°C. 

The  'pain  sense  is  tested  by  pricking  the  skin  with  needles  or  the 
sharp  points  of  an  sesthesiometer.  The  faradic  battery  with  metal 
points  or  a  wire  brush  may  also  be  used.  Instruments  for  pinching 
the  skin  and  measuring  the  sensibility  by  the  strength  of  the  pinch 
have  been  devised.  The  power  of  localizing  pain  is  lessened  in  propor- 
tion to  the  analgesia.  Pain  and  temperature  sense  are  usually  affected 
together. 

The  'paiii  sensation  of  muscles,  is  tested  by  passing  the  faradic  current 
through  the  part  or  by  deep  hard  pressure  into  the  muscle. 

The  epicritic  and  protopathic  sensibility  as  described  under  symptoms 
are  tested  practically  by  cotton-wool  giving   light-contact   sense   and 


Fig.  28. — Author's  sesthesiometer. 

pin  pricks  giving  sharp  pain  sense.  The  tests  give  an  indication  of  the 
degree  and  location  of  peripheral  nerve  injury  (Head). 

The  vibration  sense  is  tested  by  placing  a  low-pitched  tuning-fork 
upon  the  bony  prominences.  The  feeling  of  vibration  thus  communi- 
cated varies  about  as  does  the  tactile  sense,  but  it  is  said  to  be  lost  in 
diseases  in  which  the  spinal  roots  are  involved,  such  as  tabes  and  in 
serious  transverse  lesions  of  the  cord. 

The  tactile  sense,  as  well  as  the  other  special  and  the  general  sensa- 
tions, may  show  a  delay  in  conduction.  The  tactile  and  pain  sense  es- 
pecially should  be  tested  on  this  point.  The  delay  may  amount  to  several 
seconds.     It  is  especially  characeristic  of  tabes  dor  sails. 

The  stereognostic  sense  is  tested  by  placing  variously  shaped  objects 
in  the  patient's  hands  and  asking  him  to  name  them.  It  depends  upon 
the  integrity  of  the  tactile  or  of  the  deep,  i.e.,  musculo-articular,  sen- 
sibility or  upon  that  of  the  stereognostic  centre  in  the  parietal  lobe. 

The  normal  nerve-supply  of  the  skin  is  shown  in  Figs.  26  and  27. 

Tests  for  Deep  Sensibility. — Anaesthesia  of  the  special  sensory  nerves 
of  the  muscles,  joints  and  tendons  causes  ataxia  and  inco-ordination. 
Muscle  anaesthesia  causes  chiefly  a  loss  of  weight  sense  or  loss  of  power  to 
determine  weights.     It  is  tested  by  the  use  of  weights  suspended  by  a 


56  DISEASES    OF    THE    NERVOUS    SYSTEM 

string  so  as  to  exclude  pressure  sense ;  also  by  causing  the  patient  to  squeeze 
a  dynamometer  up  to  a  certain  fixed  number. 

In  articular  and  tendinous  anaesthesia  there  is  loss  of  posture  sense. 
It  is  tested  bj^  the  physician's  moving  the  patient's  limbs  and  having 
the  blindfolded  patient  tell  in  what  direction  the  movement  is  made. 
Or  he  is  told  to  follow  with  one  limb  the  movements  which  the  examiner 
makes  with  the  other,  or  the  patient  shuts  his  eyes  and  tries  to  put  the 
tip  of  his  finger  to  the  tip  of  his  nose  (finger-nose  -test)  or  the  heel  of  one 
foot  on  the  patella  of  the  other  leg  (heel-knee  test). 

Muscular,  articular  and  tendinous  anaesthesia  usually  exist  together; 
Such  ataxia  shows  itself  in  standing  and  in  locomotion  and  other  voluntary 
movements.  Thus  we  have  a  static  ataxia  and  locomotor  or  motor  ataxia. 
Static  ataxia,  or  inability  to  stand  (or  sit)  without  swaying  or  irregular 
movements,  is  tested  by  making  the  patient  stand  with  the  eyes  closed 
and  the  heels  and  toes  close  together.  Normally,  the  head  moves  not 
over  an  inch  in  this  position,  and  the  patient  holds  the  head  and  body 
more  rigid  with  the  eyes  closed  than  with  them  opened.  In  ataxic 
states  the  reverse  is  true,  and  decided  swaying  or  even  complete  loss  of 
equilibrium  occurs  with  the  eyes  closed,  or  even  with  the  eyes  open,  and 
the  base  narrowed  by  putting  the  feet  together.  This  phenomenon  is 
called  the  "Brauch-Romberg  symptom."  In  static  ataxia,  muscular  and 
articular  sensations  are  both  involved. 

Ataxia  of  motion  is  tested  by  observing  the  gait  and  the  movements  of 
the  extremities.  The  patient  cannot  walk  a  straight  line  and  cannot 
walk  without  watching  the  floor  with  the  eyes.  The  arms  cannot  be 
moved  in  a  co-ordinate  way.  With  the  eyes  closed,  the  patient  cannot 
place  the  finger  on  the  tip  of  the  nose  or  lobe  of  the  ear  or  any  indicated 
spot.  Ataxia  of  motion  involves  especially  the  articular  and  tendinous 
sensations,  but  not  these  exclusively.  It  may  be  measured  by  noting 
how  close  in  walking  the  patient  keeps  upon  a  given  line  10  feet  long; 
how  near  he  can  place  the  finger  upon  a  centre  of  a  board  marked  like 
a  target.  The  patient  is  placed  10  feet  away  and  made  to  walk  directly 
at  it  and  place  the  finger  in  the  centre. 

Hypotonia  or  loss  of  muscular  tonus  is  tested  by  having  the  patient 
lie  on  a  couch.  The  physician  takes  the  foot  and  lifts  the  leg  by  it,  the 
knee  being  kept  stiff.  Ordinarily  the  leg  cannot  be  carried  quite  to  a 
right  angle  without  the  knee  bending.  If  it  does  go  to  a  right  angle  or 
beyond,  there  is  hypotonia  of  the  limb.  The  fingers,  wrists,  toes,  ankles, 
knees  show  also  abnormal  flexibility.  This  condition  is  natural  to  some 
extent  in  children  and  it  is  sometimes  a  physiological  characteristic  of  the 
adult. 

Cerebellar  and  Vestibular  ataxia  or  asynergy.- — Ataxia  of  gait  and  station 
may  be  caused  by  lesions  of  the  cerebellum  and  its  connecting  paths, 


DIAGNOSIS    AND    METHOD    OF    EXAMINATION  57 

and  of  the  vestibular  nerve.  These  impair  the  apparatus  of  equihbrium 
and  cause  uncertain,  jerky,  staggering  movements  resemljling  some- 
what the  ataxia  above  described.  The  co-ordination  of  the  arms  is  also 
involved.  The  tests  and  description  of  cerebellar  and  vestibular  asynergy 
will  be  given  under  the  description  of  cerebellar  disease. 

Besides  the  foregoing  methods  of  examination  and  testing  for  nervous 
conditions,  there  are  a  number  of  epinomic  tests  which  are  of  impor- 
tance in  investigating  certain  special  neuroses.  I  have  put  the  de- 
scription of  these  tests  in  connection  with  the  disease  to  which  they  are 
related;  but  the  following  list  of  the  tests  collated  for  me  by  Dr.  H.  W. 
Frinck  is  given  here  as  a  matter  of  convenience  in  reference: 

Abadie's  Sign  (of  Tabes)  Mendel-Bechterew    Test    (of    Vy.    Tract 

Babinski's  Test  (of  Chronic  Paralysis)  lesion) 

Barany's  Test  (of  the  Labyrinthine  Reflex)  Moebius's  Sign  (of  Exophthalmic  Goitre) 

Biernacki's  Test  (of  Tabes)  Quinquard's  Sign  (of  Chronic  Alcoholism) 

Brissaud's  Test  (of  Organic  Paralysis)  Rinne's  Test  (of  Hearing) 

Brudzinski's  Neck  Sign  (of  Meningitis)  Romberg's  Sign  (of  Ataxia) 

Chvostek's  Sign  (of  Tetany)  Rosenbach's  Sign  (of  Hemiplegia) 

Erb's  Sign  (of  Tetany)  Schwabach's  Test  (of  Nerve  Deafness) 

Grasset's  Test  (of  Hemiplegia),  Stellwag's  Sign  (of  Exophthalmic  Goitre) 

Hoover's  Sign  of  (Hemiplegia)  Trousseau's  Sign  (of  Tetany) 

Kernig's  Sign  (of  Meningitis)  Von     Graefe's    Sign     (of    Exophthalmic 

Mannkopf's  Sign    (of  Simulated  Tender-      Goitre) 

ness)  Weber's  Test  (of  Hearing) 

McEwen's  Sign  (of  Hydrocephalus)  Wernicke's  Hemiopic  Pupillary  Reaction 

Sense  of  Vision,  Hearing,  Vestibular  Sense,  Smell  and  of  Taste. — 
See  Cranial  Nerves. 

Examinations  of  the  X-ray  are  useful  in  determining  the  presence 
of  fractures,  bony  growths,  atrophies  and  deformities.  Occasionally 
the  X-ray  photograph  helps  in  the  recognition  of  brain  tumors. 

Blood  examinations  are  necessary  in  acute  inflammatory  conditions, 
syphilis,  pernicious  anaemia,  etc.  It  is  hardly  necessary  to  speak  of  the 
need  of  tests  of  the  urine  or  of  those  which  inform  us  regarding  condi- 
tions in  the  gastro-intestinal  tract.  In  many  forms  of  nervous  diseases 
every  organ  and  fluid  of  the  body  must  be  examined  so  that  the  laboratory 
is  an  especially  important  aid  to  neurological  diagnosis. 

Examination  of  the  Cerebros'pinal  Fluid. — The  cerebrospinal  fluid  is 
normally  a  clear  liquid  with  a  specific  gravity  of  1006  to  1008.  It  is 
alkaline  in  reaction  and  contains  a  trace  of  serum-globulin  and  a  sub- 
stance which  reduces  Fehling's  solution.  There  may  be  one  or  two 
lymphoid  and  epithelial  cells.  In  certain  nervous  diseases,  such  as 
tabes,  spinal  syphilis,  paresis  and  in  inflammatory  diseases,  various 
changes  are  found.  The  special  characteristics  are  referred  to  under  the 
different  diseases. 


58 


DISEASES    OF    THE    NERVOUS    SYSTEM 


The  technic  of  spinal  puncture  as  illustrated  and  described  for 
me  by  Dr.  MacRoberts  of  the  New  York  Neurological  Institute  is  as 
follows:  The  cerebrospinal  fluid  can  be  obtained  in  a  safe  and  simple 
manner  by  introducing  a  long  hollow  needle  equipped  with  a  stylet  through 
the  dura  mater  in  the  lumbar  region  of  the  spine.  The  needle  is  specially 
constructed  for  this  purpose.  The  Hastings  needle,  the  one  generally 
used,  is  of  strong  flexible  steel  of  fine  bore  with  a  handle  large  enough  to 
allow  of  firm  grasp. 

The  needle  should  be  boiled  and  the  operation  carried  out  under 
sterile  precautions. 

The  patient  is  best  seated  on  a  chair  or  the  edge  of  his  bed  with  his 
back  rounded  toward  the  operator.     If  weak  or  unable  to  sit  up  he  may 


Fig.  29. — Spinal  puncture.     The  needle  is  inserted  along  the  lower  edge  of  a  spinous 
process  marked  by  the  tip  of  the  thumb. 

lie  on  his  side  with  knees  drawn  up  toward  his  chest.  In  cases  of  brain 
tumor  or  of  greatly  increased  intracranial  pressure  the  patient  should  be 
on  his  side.  In  cases  of  posterior  fossa  tumor  or  marked  distention  of 
the  ventricles  the  puncture  can  be  performed  with  comparative  safety 
if  the  foot  of  the  bed  be  first  elevated  with  shock  blocks  and  allowed 
to  remain  in  this  position  for  eight  hours  or  more  after  the  withdrawal 
of  the  fluid. 

It  has  been  found  advisable  to  tell  the  patient  in  a  few  simple  words 
what  is  about  to  be  done,  saying  that  he  may  expect  the  pain  of  a  pin 
prick  as  the  needle  goes  through  the  skin,  but  if  he  then  keep  very  still 
the  remainder  of  the  procedure  can  be  completed  in  a  few  moments 
without  causing  him  further  pain. 


DIAGNOSIS    AND    METHODS    OF    EXAMINATION 


59 


The  point  of  election  for  the  insertion  of  the  needle  is  between  the 
third  and  fourth  or  fourth  and  fifth  lumbar  vertebrae,  in  the  median  line 
or  slightly  to  one  side.  The  location  is  best  obtained  by  making,  with 
an  applicator  dipped  in  tincture  of  iodine,  a  straight  line  which  unites 
the  iliac  crests.  Where  this  line  crosses  the  line  of  the  spinous  processes 
a  space  between  the  spines  will  be  found  by  palpation  with  the  thumb. 
The  skin  about  this  point  should  be  sterilized  with  alcohol  and  tincture  of 
iodine.  The  thumb  of  the  left  hand  should  be  placed  on  the  spinous 
process  above  the  interspinous  space  with  the  edge  of  the  thumb  even 
with  the  lower  edge  of  the  bone.     The  needle  should  be  grasped  firmly 


Fig.  30. — Spinal  puncture.     Showing  tlie  position  of  the  patient  and  the  position  of 
operator's  thumb  palpating  the  lower  edge  of  a  spinous  process. 

with  the  base  against  the  palm  and  the  shaft  steadied  with  the  fingers,  and 
the  point  placed  just  below  the  thumb  edge  and  thrust  smartly  through 
the  skin.  It  may  then  be  more  slowly  pushed  through  the  ligamentous 
structures  until  by  the  change  in  resistance  it  can  be  felt  to  have  pierced 
the  dura  mater.  The  stylet  should  then  be  withdrawn  and  4  or  5  cc. 
of  the  fluid  collected  in  a  sterile  test-tube.  The  needle  is  then  carefully 
but  quickly  removed  and  a  small  square  of  gauze  fastened  over  the 
puncture  point  with  adhesive. 

The  fluid  should  be  corked  and  placed  in  the  ice  box  and  should  be 
examined  some  time  within  the  next  twenty-four  hours. 

Following  the  puncture  it  has  been  the  custom  to  have  the  patient 
lie  flat  on  his  back  for  twenty-four  hours.  It  has  been  found  recently 
that,  by  allowing  our  patients  up  sooner,  fewer  headaches  resulted. 

The  fluid  is  later  tested  for  blood,  excess  of  globulin,  the  Wassermann 
reaction,  the  number  and  character  of  cells,  cholin,  sugar,  and  bacteria. 
The  special  methods  and  indications  are  given  under  the  description  of 
meningitis,  syphilis,  cerebral  hemorrhage  and  cerebral  abscess,  and  cord 
tumors. 


CHAPTER  VI 
HYGIENE,  PROPHYLAXIS,  TREATMENT 

In  the  treatment  of  nervous  disease,  the  physician  attempts  to 
relieve  distressing  symptoms,  to  secure  radical  cure,  and  to  prevent 
return.  This  calls  for  various  measures  which  may  be  classed  under 
the  heads  of  general  hygiene,  diet,  exercise,  climate,  hydrotherapy,  mas- 
sage in  various  forms,  electricity,  drugs,  external  applications  and 
surgical  intervention. 

General  Hygiene. — To  secure  and  keep  steady  nerves  and  to  pre- 
vent the  supervention  of  organic  nervous  disease,  would  require  a 
considerable  reconstruction  of  the  present  social  system.  The  struggle 
for  existence  and  success  is  keener  than  it  used  to  be.  There  is  a  smaller 
field  for  the  slightly  backward  class,  and  more  men  fail  in  life  and  become 
parasitical  than  formerly  when  there  was  a  wider  field  for  the  simpler 
manual  occupations. 

I  can  only  give  some  hints  as  to  the  kind  of  advice  physicians  should 
give  to  help  along  those  who  are  very  likely  to  be  handicapped  by  a 
neuropathic  constitution.  Thus  two  people  of  very  nervous  tempera- 
ment or  bad  stock  should  not  marry.  Blood  relations  of  the  same  tem- 
perament should  not  marry,  and  families  with  a  psychopathic  taint  should 
not  intermarry.  Children  should  be  brought  up  to  eat  slowly  a  mixed 
diet,  to  sleep  early  and  long,  to  play  in  the  open  air,  to  learn  self-control 
and  obedience.  Their  parents  should  keep  from  them  all  infective  fevers. 
Systematic  study  and  work  are  good  for  all  children.  It  is  the  strain 
due  to  defective  vision,  poor  light  and  ventilation  and  unsuitable  tasks 
that  hurts  the  neurotic.  Education  and  occupation  are  the  best  kind 
of  builders  up  of  healthy  nerves.  There  are  children,  however,  who 
cannot  follow  the  ordinary  educational  lines  and  who  must  be  specially 
trained  in  consequence.  The  queer  and  eccentric  children  with  some 
twist,  or  precocious  talent,  need  especial  care.  They  usually  must  be 
brought  up  to  follow  lives  on  a  low  mental  plane.  Too  many  good 
farmers  and  artisans  are  spoiled  by  being  made  poor  professional  men, 
or  being  set  up  in  responsible  business  positions.  Adults  need  to  keep 
in  mind  especially:  moderation,  exercise  and  the  avoidance  of  a  luetic 
infection.  With  these  most  need  not  fear  the  use  of  alcohol,  tobacco, 
tea,  coffee,  or  even  occasional  irregularities  in  sleeping  and  eating.  Phys- 
ical and   mental   strains,  infective   fevers  and  toxins  are   prolific   pro- 

60 


HYGIENE,    PROPHYLAXIS,    TREATMENT  61 

moters  of  nervous  disease.  Syphilis  stands  out  as  the  most  important 
single  factor  in  producing  organic  nervous  diseases.  If  it  could  be  re- 
moved we  would  have  no  locomotor  ataxia,  or  paresis,  less  myelitis,  and 
far  fewer  cases  of  apoplexy. 

Alcohol  is  a  less  important  factor,  but  does  much  to  produce  mental 
disease,  vascular  disease,  and  hereditary  degeneration. 

Diet. — There  is  no  definite  formula  for  diet  in  nervous  diseases. 
The  kinds  of  foods  which  are  suitable  for  infants  and  children,  and 
growing  youths,  are  not  equally  suitable  for  the  mature  or  the  senile. 
There  are  some  general  facts,  however,  which  may  be  laid  down,  re- 
garding the  diet  for  the  nervous;  that  is  to  say,  for  persons  who  have 
a  more  or  less  neurotic  and  unstable  constitution.  This  class  of  per- 
sons seems  to  be,  as  a  rule,  unable  to  tolerate  sweets  or  large  amounts 
of  flesh  food,  and  they  do  best  upon  a  mixed  diet  which  contains  a 
moderate  amount  of  proteid  together  with  vegetables  and  fruit.  The 
question,  whether  neurotic  patients  do  better  upon  the  so-called  "high" 
proteid  of  flesh  or  the  "low"  proteid  of  vegetables,  does  not  seem  yet 
to  be  settled,  though  the  practice  is,  on  the  whole,  rather  more  in  favor  of 
using  the  flesh  proteid  than  the  vegetable  proteid,  especially  in  the  early 
half  of  life. 

There  are  four  kinds  of  what  may  be  called  general  diets  prescribed 
for  patients.  I  do  not  mean  to  include  in  these  four,  however,  the 
special  diets  that  are  used  in  the  acute  and  organic  diseases,  such  as 
diabetes  and  fevers,  serious  gastric  disturbances,  and  so  on. 

These  four  diets  are :  first,  vegetarianism ;  second,  the  modified  vege- 
tarian or  purin-free  diet;  third,  the  Salisbury  high-proteid  diet,  and, 
fourth,  the  Chittenden  or  "low  diet." 

The  pure  vegetarian  diet  is  one  which  has  no  scientific  basis,  and 
which  seems  to  me,  on  the  whole,  as  unwise,  though  it  apparently  suits 
certain  constitutions,  and  is,  if  anywhere,  especially  suitable  for  those 
of  rather  advanced  years. 

The  purin-free  diet  is  vegetarianism  plus  the  use  of  milk  and  cheese. 
In  this,  there  is  a  reduction  of  the  proteicls,  but  an  increase  somewhat,  of 
the  fats  and  carbohydrates. 

The  Salisbury  diet  consists  of  lean  beef  and  hot  water,  and  its  use 
involves  a  large  increase  of  the  proteids  and  of  the  purin-bodies,  while 
there  is  a  decrease  of  the  fats  and  carbohydrates.  This  diet  is  usually 
somewhat  modified  by  the  addition  of  bread  or  toast,  and  sometimes 
of  fruits,  so  that  the  diminution  in  the  carbohydrates  is  not  so  marked. 

The  Chittenden  diet  is  one  in  which  the  food,  as  a  whole,  is  cut 
down  in  all  its  forms,  the  proteid  being  reduced  nearly  one-half.  Ex- 
perience has  shown,  that  all  these  different  diets  may  lead  to  the  same 
therapeutic  results — that  is  to  say,  that  a  purin-free  diet  will  cure  a  mi- 


62  DISEASES    OF    THE    NERVOUS    SYSTEM 

graine  or  lessen  the  attacks,  and  that  a  Sahsbury  or   meat  diet  may 
do  the  same. 

The  injmy  caused  by  any  form  of  diet  is  largely  due  to  the  fact  that 
putrefactive  changes  occur  in  it,  leading  to  toxaemias,  or  that  there  gets 
into  the  blood  an  excess  of  food  or  fuel;  and  if  this  diet  is  modified  so  that 
such  an  excess  is  lessened,  without  weakening  the  system,  we  can  secure 
good  results.  In  fine,  the  main  factor  in  prescribing  any  diet,  is  to  see 
that  it  is  a  digestive  and  assimilable  one,  and  that  there  does  not  get  into 
the  system  an  excess  of  fuel,  producing  what  is  termed  a  ''hyperpyrsemia." 

In  elderly  persons  the  amount  of  nitrogenous  food  needed  in  the  form 
of  meat  is  usually  less;  and  they  often  do  well  on  a  vegetarian  diet. 
As  a  rule,  however,  vegetarians  after  a  few  years  find  that  a  return  to 
some  carnivorous  food  is  indicated. 

Some  neurotic  persons  seem  to  need  a  great  deal  of  food  but,  as  a 
rule,  harm  comes  from  full  diets  and  one  cannot  get  strong  by  stuffing. 

The  frankly  nervous,  the  hypomanic  and  psychasthenic  patients  should 
not  use  alcohol  at  all.  Tea  and  coffee  can  be  taken  in  very  small  amount 
and  best  without  sugar.  The  various  alkaline  mineral  waters  may  be 
used  temperately  with  impunity,  but  none  of  them  have  much  specific 
effect  in  relieving  nervousness  or  curing  the  nervous  temperament. 

Exercise. — ^As  a  prophylactic  against  nervous  disorders,  the  value  of 
exercise,  especially  if  taken  out  of  doors,  can  hardly  be  overestimated. 
Brain  workers  are  better  for  moderate  exercise,  but  they  do  not  need 
much;  and  after  twenty-five,  severe  intellectual  work  can  rarely  be  done 
by  persons  in  athletic  training.  Before  the  age  of  twenty-five,  when  the 
system  is  exuberant  with  vitality,  hard  study  and  hard  physical  exercise 
can  be  pursued  successfully'-  together  by  some.  Persons  of  a  neuropathic 
constitution  are  most  benefited  by  regular  exercise  when  it  interests  the 
mind.  Indoor  gymnasium  exercise  with  the  ordinary  apparatus  does 
little  good  except  through  the  bath  that  follows  it.  In  many  forms  of 
chronic  organic  nervous  disease,  exercise  is  to  be  prohibited. 

The  most  important  line  of  effort  in  prophylaxis  is  the  warding  off 
of  excessive  or  premature  arteriosclerosis.  The  surest  preventive  of  this 
is  a  good  heredity.  But,  given  an  average  constitution,  one  can  delay 
arterial  degeneration  only  by  leading  a  perfect  life,  that  is  to  say,  the  in- 
dividual must  avoid  all  mental  and  physical  strain  and  shock,  alcohol, 
excesses  in  eating  and  tobacco.  He  must  not  get  syphilis.  He  must 
keep  the  emunctories  open  and  get  as  much  as  possible  of  fresh  air.  All 
of  which  is  the  council  of  perfection,  except  for  children.  Here  wise  parents 
can  do  much  to  prevent  the  development  of  arterio-sclerotic  neuroses. 

Hydrotherapy. — Hydrotherapy  is  the  science  of  applying  water  in  the 
treatment  of  disease.  The  modes  by  which  it  is  used  in  neurological 
therapeutics  are: 


HYGIENE,    PROPHYLAXIS,    TREATMENT  63 

I.  General  hydrotherapy: 

1.  Tonic  hydrotherapy. 

2.  Sedative  hydrotherapy. 

3.  Indifferent  baths  for  mechanical  purposes. 

II.  Local  hydrotherapy. 

The  details  of  the  use  of  these  measures  are  now  eml)odied  in  special 
treatises  and  works  on  therapeutics. 

Massage. — -The  term  massage  may  be  made  to  include  all  the  manipu- 
lations of  the  body  for  the  purpose  of  curing  disease.  The  different 
methods  of  applying  it  as  classified  by  Jacoby  are : 

Effleurage  or  gentle  stroking.  The  maximum  force  to  be  applied 
here  should  not  exceed  the  weight  of  the  hand.  Massage  a  friction  or 
rubbing.  Energetic  strokes  with  one  hand  and  strong  circular  or  to- 
and-fro  friction  with  the  other.  Petrissage  or  kneading.  Tapoiement 
or  percussion  with  the  fingers,  hands,  or  instruments.  Frictional  move- 
ments, passive,  active  and  combined  with  movements  are  made  by  the 
operator.  The  physician  may  be  reminded  that  a  male  operator  is  a 
masseur,  a  female  a  masseuse,  and  that  the  patient  is  massed. 

Massage  accelerates  the  lymph  and  venous  currents,  and  thus  pro- 
motes absorption.  It  increases  at  least  temporarily  the  number  of  red 
blood-cells  (Mitchell).  It  increases  the  rapidity  and  force  of  the  heart 
beat  (except  abdominal  massage  which  slows  the  heart)  and  helps  to 
relieve  local  congestions  and  inflammatory  deposits.  It  presses  and 
stretches  the  terminal  nerve  filaments,  increases  the  irritability  of  motor 
nerves  and  the  contractility  of  muscles.  It  may  either  increase  or  lessen 
the  irritability  of  sensory  nerves  according  as  it  is  applied.  Of  the  various 
forms  of  massage,  tapotement  is  frequently  useful  and  is  the  kind  often 
used  in  neuralgias.  It  is  applied  not  only  with  the  fingers  and  hand, 
but  also  by  the  aid  of  rubber  tubes  known  as  muscle  beaters,  rubber  balls 
with  rattan  or  whalebone  handles,  percussion  hammers  and  various 
percuteurs. 

Massage  is  of  considerable  value  in  certain  forms  of  atonic  neuras- 
thenia and  hysteria  associated  with  anaemia,  dyspepsia  and  feeble  circu- 
lation; in  hemiplegia,  in  the  paralyses  of  peripheral  origin,  in  functional 
spasm,  especially  in  some  forms  of  writer's  cramp  and  allied  neuroses, 
in  cerebral  hypersemia,  insomnia,  constipation  and  in  headache  and  some 
neuralgias,  especially  those  about  the  head,  neck,  and  arm.  It  is  con- 
traindicated  usually  in  heart  disease,  in  advanced  arteritis  or  when  there 
is  danger  of  dislodging  a  thrombus. 

Regular  educational  muscular  movements  according  to  a  certain  fixed 
schedule  are  used  in  the  treatment  of  locomotor  ataxia  and  paralysis. 
The  details  of  these  exercises  will  be  given  later. 


64  DISEASES    OF    THE    NERVOUS    SYSTEM 

Osteopathy. — ''A  system  of  therapeutics  based  upon  the  theory  that 
many  diseases  are  due  to  pressure  upon  the  vessels  or  nerves  by  some  dis- 
placed vertebra  or  other  part  of  the  skeleton,  or  to  a  condition  of  imbalance 
of  the  muscles  moving  any  joint;  the  treatment  is  directed  to  the  me- 
chanical correction,  by  means  of  manipulation,  of  the  assumed  osseous 
displacement  or  muscular  imbalance,  with  the  consequent  repression  of 
the  abnormal  reflexes  and  a  restoration  to  normal  of  the  circulation  and 
the  nerve  impulses"  (Stedman). 

It  is  a  form  of  treatment  which  gets  results,  according  to  my  experience 
partly  by  suggestion  and  partly  by  improving  mechanical  conditions,  as 
does  massage.  It  is  dangerous  in  certain  forms  of  nervous  disease  like 
tabes.  It  is  useless  in  others  like  Parkinson's  disease.  It  is  dangerous 
also,  like  all  special  therapeutic  systems,  when  it  makes  large  and 
unfounded  claims. 

Climate  in  Nervous  Diseases. — The  factors  which  make  up  a  special 
kind  of  climate  are:  Purity  of  air;  temperature;  humidity;  sunlight; 
rarefaction  of  air;  ozone;  wind;  electricity;  soil;  trees,  social  conditions. 

Regarding  these  points,  some  facts  are  very  well  settled.  The  air 
in  the  country  is  purer  than  in  cities.  The  air  on  the  sea  and  at  high 
levels  is  purer  than  in  other  localities.  The  temperature  above  the  sea 
level  chminishes  about  1°F.  for  every  300  to  350  feet,  and  is  less  the 
dryer  the  air.  Alterations  in  temperature  are  less  near  the  sea  and  less 
in  the  southern  hemisphere.  The  higher  the  elevation  and  the  colder  the 
air,  the  less  moisture  does  it  contain.  About  the  factors  of  ozone  and  elec- 
tricity in  the  air  little  definite  is  known.  As  to  sunlight,  an  excessive 
amount  of  it  is  said  eventually  to  enervate  patients. 

Climates  are  classified  by  Weber  into  marine,  low-level  inland  and 
high-level  inland.  These  all  have  great  variations  in  quality,  depend- 
ing upon  their  temperature,  moisture,  etc.  As  a  general  rule,  warm 
marine  climates  and  sea  voyages  are  best  for  neurasthenic  invalids  of 
the  irritable  type.  On  the  other  hand,  in  atonic  and  anaemic  con- 
ditions high  inland  climates  are  better,  at  least  for  a  time.  Such  climates 
should  not  be  too  dry  or  windy. 

In  organic  degenerative  diseases  of  the  nervous  system,  marine 
climates  and  low  levels  are  better.  As  a  whole,  it  seems  to  be  the  con- 
clusion that  plenty  of  fresh  air  is  the  essential  in  all  climates  and  is 
better  than  any  special  climates.  Relatively  short  changes  from  low 
to  high  levels  or  from  temperate  to  tropic  climates  often  leave  a  distinctly 
tonic  effect. 

Germany,  the  Riviera,  the  Bermudas,  the  Azores,  the  West  Indies, 
southern  Colorado,  Arizona  and  southern  California  are  favorite  places 
for  sending  neurasthenic  Americans.  Camp  life  in  the  Adirondacks  or 
other  forests  is  also  found  most  useful. 


HYGIENE,    PROPHYLAXIS,    TREATMENT  65 

ELECTRICITY  IN  NERVOUS  DISEASES 

Technical  Terms. — -There  are  certain  technical  terms  which  it  is 

necessary  to   understand.     Electromotive  force    (symbol,    EMF)    is   the 

force  which  tends  to  set  electricity  in  motion.     An  electric   current 

results.     The  current  strength  (symbol,  C)  is  the  term  used  to  express 

the  capacity  of  the  separated  fluids  to  overcome  resistance  in  their 

attempts   to   reach   equilibrium   or   equalization   again.     This    current 

strength,  or  simply  the  current,  naturally  is  in  proportion  to  the  strength 

of  the  electromotive  force,  which  is  constantly  dissociating  the  electrical 

fluids  and  generating  the  current.     If,  however,  as  is  always  the  case, 

the  electrical  fluid  meets  resistance  in  seeking  equilibrium,  the  resistance 

diminishes  its  current.     Hence  we  have  the  formula  known  as  Ohm's 

law: 

„          X    X        XI          Electromotive  force         „       EMF. 
Current  strength  = ^ — ^- ;  or  L  =  — ^ — 

All  bodies  offer  some  resistance  to  electrical  currents,  and  it  is  im- 
portant to  have  some  standard  unit  of  resistance  for  the  sake  of  com- 
parison. Such  standard  unit  has  been  adopted  and  is  called  an  ohm. 
It  is  the  resistance  offered  to  a  current  by  a  certain  piece  of  wire  of  definite 
size  and  length. 

A  volt  is  the  unit  of  electromotive  force,  i.e.,  it  represents  the  force 
which  will  generate  a  certain  amount  of  electricity  in  a  second  of  time. 
A  Daniell  cell  is  not  quite  one  volt  strength. 

An  ampere  is  the  unit  of  working  power  or  current  strength.  It 
is  the  current  strength  produced  by  one  volt  of  electromotive  force 
working  against  one  ohm  of  resistance.  A  milliampere  is  one-thou- 
sandth of  an  ampere.     A  watt  is  the  unit  of  work. 

When  a  given  current  flows  along  from  a  large  into  a  small  con- 
ductor, the  quantity  in  this  latter  conductor  in  a  given  section  is  greater 
and  the  current  is  said  to  be  denser.  The  instrument  by  which  the 
strength  of  a  current  is  measured  is  known  as  the  amperemeter;  in 
medical  practice,  only  fractions  of  the  ampere  are  used,  and  the  in- 
strument is  called  the  milliamperemeter.  A  rheostat  is  an  instrument 
for  interposing  resistance  in  a  current. 

Electrical  Appliances. — -The  batteries  used  in  neurological  practice 
are:  the  static,  the  faradic,  the  galvanic,  and  the  high  frequency. 

The  current  of  the  faradic  battery  varies  in  quality  in  accordance, 
(1)  with  the  length  and  number  of  turns  in  the  coil;  (2)  the  form  of  the 
electrical  wave;  (3)  the  number  of  interruptions;  and,  (4)  the  strength  of 
the  battery. 

The  currents  from  short  coils  of  coarse  wire  have  a  lower  potential 
and  slightly  more  voltage.     They  are  more  eflicient  in  producing  mus- 

5 


66 


DISEASES    OF    THE    NERVOUS    SYSTEM 


cular  contractions  and  are  more  irritating  to  the  sensory  nerves.  These 
qualities  are  increased  with  slow  interruptions  of  three  or  four  per 
second.  When  muscular  contractions  and  mechanical  exercise  with 
stimulation  are  desired,  the  short  coils  (primary  or  secondary)  with 
slow  interruptions  are  indicated.  The  current  from  long  coils  has  a 
higher  potential  and  less  voltage;  it  has  less  power  in  contracting  muscles 
and  a  different  effect  on  the  sensory  nerves.  When  the  interruptions 
are  very  rapid  and  the  coil  is  very  long,  the  effect  on  the  sensory  nerves 
seems  more  sedative;  perhaps,  in  part,  because  of  a  change  in  the  form  of 
the  electrical  waves. 

The  physiological  effect  of  a  current  depends,  as  I  have  stated, 
in  part  upon  the  character  of  the  wave  of  electrical  force.  If  this  is 
high  and  sharp,  the  stimulation  is  different  from  that  produced  by 


Fig.  31. — Author's  electrode  set. 

a  wave  which  gradually  rises  to  its  height.  D'Arsonval  has  devised  an 
instrument  for  producing  these  blunt-topped  waves,  and  at  the  same  time 
reversing  the  current.  The  current  is  called  sinusoidal.  I  am  not 
aware  of  any  special  therapeutic  results  in  neurology  from  this  kind  of 
current,  though  it  is  claimed  that  very  slow  wave-like  currents  affect 
better  involuntary  muscles.  The  Leduc  current  is  a  rapidly  interrupted 
galvanic  current,  the  period  of  duration  of  the  current  being  one-tenth 
that  of  the  intermission.  It  is  claimed  that  when  sufficiently  powerful, 
20  to  60  volts  or  more,  it  produces  local  anaesthesia  and  when  passed 
through  the  head  to  produce  general  ansesthesia  and  sleep. 

Very  rapidly  interrupted  and  alternated  currents  of  extremely 
high  voltage  are  called  high  frequency  currents.  When  passed  through 
the  entire  body  they  lower  blood  pressure  5  to  10  points,  and  increase 
metabolism.  When  applied  locally  under  the  name  of  "violet-ray" 
curents  they  have  an  efficient  counterirritant  effect. 


HYGIENE,    PROPHYLAXIS,    TREATMENT  67 

Galvanic  Batteries. — -The  ordinary  accessories  to  tlie  faradic  and 
galvanic  batteries  are  electrodes,  rheostat  and  milliamperemeter. 

The  electrodes  needed  for  ordinary  purposes  are:  An  indifferent 
electrode  measuring  5  cm.  by  15  cm.  A  normal  electrode,  10  sq.  cm. 
A  unit  electrode,  1  sq.  cm.  A  soft  wire  brush.  Three  handles:  one 
10  cm.  and  one  40  cm.  long,  one  short  handle  with  an  interrupter.  A 
milliamperemeter.     A  rheostat.     (See  Fig.  33.) 

Methods  of  Application. — Static  electricity  is  applied  for  fifteen 
or  twenty  minutes  daily  or  tri-weekly.  For  general  tonic  or  sedative 
effects,  sparks  are  drawn  from  all  parts  of  the  body  except  the  face. 
In  paralysis  or  spasm  or  pain,  sparks  are  applied  to  the  affected  area. 
For  headaches  and  cerebral  parsesthesise  the  electrical  breeze  is  very 
useful,  but  it  must  be  strong. 

The  faradic  and  galvanic  currents  are  used  for  about  the  same  time 
and  intervals  as  the  static.  In  some  cases,  however,  the  galvanic 
current  should  be  given  daily  or  even  two  or  three  times  a  day.  As  a 
rule,  a  course  of  electrical  treatment  should  be  continued  for  six  to  eight 
weeks,  and  then  discontinued  for  a  time. 

In  general  electrization,  whether  galvanic  or  faradic,  the  indifferent 
electrode  is  placed  on  the  sternum,  feet  or  back,  and  the  other  pole 
is  carried  over  the  limbs,  trunk,  neck  and,  if  indicated,  the  head.  In 
some  cases,  however,  the  two  electrodes  are  applied  together  upon  the 
different  muscles  of  the  body.  In  local  electrization,  the  large  elec- 
trode may  be  applied  on  an  indifferent  spot  and  the  other  applied  to 
the  affected  limb  or  limbs,  or  the  two  electrodes  may  be  used  together 
on  the  same  segment  of  muscles.  There  are  special  points  at  which  the 
muscular  contraction  is  most  easily  brought  out.  These  are  called 
the  motor  points. 

Electro-diagnosis. — When  a  motor  nerve  is  cut  off  from  its  centre 
in  the  spinal  cord,  or  when  this  centre  itself  is  diseased,  the  nerve  and 
later  the  muscle  undergo  a  degeneration.  As  a  result  of  this,  their  reac- 
tion to  electrical  currents  is  changed,  and  we  get  what  is  termed  ''partial 
degeneration  reactions"  and  "complete  degeneration  reactions,"  accord- 
ing to  the  degree  of  disturbance.  These  reactions  are  due  mainly,  if  not 
wholly,  to  the  degeneration  in  the  terminal  nerve-fibres  and  motor  end- 
plates  in  the  muscle.  When  the  muscle  alone  is  diseased,  the  reaction  is 
not  changed  until  very  late.  The  change  in  irritability  is  due  to  the  fact 
that  as  the  nerve-fibre  wastes  it  takes  an  electric  current  of  comparatively 
long  duration  and  considerable  strength  to  stimulate  it. 

The  first  effect  is  to  cause  it  to  lose  its  contractility  or  reaction  to 
weak  currents,  then  to  extremely  rapid,  short  currents  like  the  static, 
then  to  the  faradic,  and  last  to  the  galvanic.  Such  change  is  known  as 
the  quantitative  alteration  in  electric  irritability. 


68  DISEASES    OF    THE    NERVOUS    SYSTEM 

But  besides  this,  the  nerve  and  muscle  are  affected  in  a  different 
way  by  the  different  poles  of  the  galvanic  battery.  In  normal  nerve 
and  muscle,  a  contraction  is  caused  more  readily  by  the  negative  pole 
than  by  the  positive.  But  muscles  with  degenerated  nerve  supply 
sometimes  respond  as  well  or  better  to  the  positive  pole.  This  forms 
what  is  called  the  qualitative  or  serial  change  in  the  irritability  of  the 
muscle. 

Finally,  degenerated  muscles  respond  more  sluggishly  than  normal 
to  the  galvanic  and  faradic  currents.  The  contraction,  instead  of 
being  sharp  and  jerky,  is  sluggish  and  almost  tetanic.  This  is  called 
the  modal  change  in  irritability,  and  it  is  far  the  most  important  sign  of 
muscular  degeneration. 

The  qualitative  change  is  gotten  only  by  placing  the  active  elec- 
trode over  the  muscle,  but  the  quantitative  and  modal  changes  may  be 
gotten  by  placing  the  electrode  over  the  nerve  as  well  as  over  the  muscle. 
In  describing  these  changes,  the  following  abbreviations  are  used: 

DeR  =  degeneration  reaction. 

AnCC  =  anode  or  positive-pole  closure  contraction. 

CaCC  =  cathode  or  negative-pole  closure  contraction. 

AnOC  =  anode  opening  contraction. 

CaOC  =  cathode  opening  contraction. 

Te  =  tetanus. 

D  =  circuit  is  closed  and  current  flowing. 

AnDTe  =  tetanic  contraction  while  the  positive  pole  is  applied 
and  the  circuit  closed. 

The  sign  >  means  greater  than;  <,less  than.  Thus  AnCC  <  CaCC 
means  anode  closure  contraction  is  greater  than  cathode  closure  contrac- 
tion. 

Degenerations  in  nerve  do  not  occur  except  in  lesions  of  the  peripheral 
motor  neuron  and  in  very  late  stages  of  primary  atrophy  of  muscles. 
Hence,  when  one  finds  degenerative  reactions  he  can  almost  absolutely 
exclude  disease  of  the  brain,  functional  disease  and  primary  disease  of 
the  muscle.  The  following  rules  may  be  formulated  for  testing  for  de- 
generation reactions : 

Use  the  faradic  current  first. 

The  Faradic  Current. — Use  a  secondary  induction  coil  of  wire  0.225  mm.  in  diam- 
eter and  800  m.  long.  The  distance  over  which  the  coil  moves  is  divided  into  a  hun- 
dred parts.     The  strength  of  current  is  indicated  by  percentage  or  millimetres. 

Record  the  minimum  necessary  for  muscular  contraction,  using  the  same  elec- 
trodes and  in  the  same  way  as  in  testing  with  galvanism. 

The  Galvanic  Current. — (1)  Place  the  indifferent  pole  over  the  sternum  and  a  10 
sq.  cm.  electrode  over  the  muscle.  (2)  Pass  the  current  for  one  minute.  (3)  Then 
find  the  minimum  strength  needed  for  a  cathode  closure  contraction.  (4)  Then  for 
an  anode  closure  contraction.     Repeat  this  test  three  times.     (5)  With  a  given  cur- 


HYGIENE,    PKOPHYLAXIS,    TREATMENT 


69 


rent,  note  whether  the  cathode  closure  contraction  is  stronger  than  AnCC  or  other- 
wise. Test  this  three  times.  (6)  Note  the  character  of  tlie  contraction,  if  sharp  or 
sluggish.     (7)  Test  nerve  in  same  way. 

The  qualitative  changes  may  be  expressed  by  a  formula  like  AnCC  =  or  >  CaCC; 
i.e.,  the  positive-pole  closure  contraction  is  equal  to  or  greater  than  the  negative-pole 
closure  contraction.  Or,  better,  the  minimum  strength  of  current  required  to  cause 
a  contraction  in  the  muscle  is  recorded  for  the  positive  pole  and  for  the  negative. 
Thus: 

AnCC  5  ma.  or  8  cells. 

CaCC  4  ma.  or  6  cells. 


Fig.  32. 


The  following  table  and  diagram  (Fig.  32)  show  the  diseases  in  which 
degeneration  reactions  may  be  expected: 

Table   Showing  the  Lesion,  its  Results,  the   Names    of  the   Diseases  and 
THE  Electrical  Reactions 


Lesion  of — 

Result 

Disease 

Electrical  Reaction  as  to 
Qualitative 

1  to  21/^. 

Paralysis, contractures. 

Hemiplegia    from    hemorrhage. 

Nerve:  normal. 

Cortex   to   cord. 

Embolism,       tumors,       lateral 
sclerosis. 

Muscle:  normal. 

3,  4  and  5. 

Paralysis,  degenerative 

Acute     and     chronic     anterior 

Nerve:  DeR. 

Cornua. 

atrophy  of  nerve  and 
muscle. 

poliomyelitis. 

Muscle:  DeR. 

2  to  5 

Paralysis,  contractures. 

Amyotrophic    lateral    sclerosis. 

Nerve:  normal 

Muscle:  normal   or   partial 

5  to  6. 

Degenerative  atrophy, 

Progressive  muscular   atrophy, 

DeR.       When     disease     is 

of  muscle. 

bulbar  paralysis. 

advanced. 

Later,  degeneration  of 

nerve. 

70 


DISEASES    OF    THE    NERVOUS    SYSTEM 


Table   Showing  the  Lesion,   its   Results,   the    Names  of  the  Diseases  and 
THE  Electric  Reactions. — {Continued) 


Lesion  of — 

I 

Result 

Disease 

Electrical  Reaction  as  to 
Qualitative 

Nerve 

Paralysis,  degenerative 

Neuritis,     from    wounds,     tox- 

Muscle: DeR. 

atrophy  of  nerve  and 

emia  or  pressure. 

muscle. 

Nerve:  DeR. 

Muscle 

Wasting,  paresis. 

Simple     atrophy;     primary     or 

Nerve   and   muscle   normal 

idiopathic  myositis.      Pseudo- 

until  late  in  the  disease. 

muscular    hypertrophy;    other 

types  of  primary  myopathies. 

Rheumatic   atrophy   and  pare- 

sis. 

It  should  be  said,  finally,  that  it  is  the  sluggish  contraction  which 
is  the  most  important  element  in  showing  degeneration;  also  that  it  is 
the  muscle  which  should  be  tested  most  carefully,  as  only  over  it  does  one 
get  the  qualitative  changes. 

Therapeutics. — ^Electricity  is  used  as  a  counter-irritant  and  as  a 
general  mechanical  tonic  in  states  of  muscular  and  nervous  weakness.  It 
is  used  in  paralysis,  spasm  and  pain,  and  for  its  supposed  specific  action  in 
certain  functional  and  organic  diseases. 

.  The  faradic  and  static  currents  have  a  counter-irritating,  stimulating 
and  excito-reflex  effect.  The  galvanic  current  has  a  sedative  and  anti- 
spasmodic effect.  The  high-frequency  current  promotes  metabolism  and 
temporarily  reduces  blood-pressure. 

The  ''violet-ray"  current  acts  mainly  as  a  counter-irritant. 

Electrolytic,  cauterizing,  and  cataphoric  effects  are  also  produced, 
but  are  rarely  needed  by  the  neurologist.  A  considerable  portion  of  the 
effects  of  electricity  are  psychical,  but  they  are  not  the  less  real  or 
valuable. 

Radiant  Energy  in  the  form  of  X-rays,  ultra-violet  rays,  radium 
emanations  have  been  of  more  help  to  surgery  than  medicine  in  thera- 
peutics. The  X-ray  and  radium  are  said  to  have  some  effect  in  neuritis 
and  neuralgia,  but  the  results  are  not  uniform  or  as  yet  conclusive. 

The  X-ray  with  the  Coolidge  tube  and  radium  have  some  effect  in 
destroying  new-growths,  and  are  being  used  in  spinal-cord  and  cerebral 
tumors. 

PSYCHOTHERAPY 

Psychotherapy  is  a  term  applied  to  that  form  of  healing  in  which 
mental  influences  are  used  to  correct  morbid  processes. 

Psychotherapeutics  has  always  been  used  in  an  irregular  and  casual 
way  to  cure  disease.  Modern  therapeutics  endeavors  to  formulate 
definite  rules  for  its  use  and  to  indicate  systematically  the  conditions 
for  which  it  should  be  applied. 


HYGIENE,    PROPHYLAXIS,    TREATMENT  71 

Hypnotism  is  the  oldest  and  best  known  method.  In  hypnotic  thera- 
peutics the  patient  is  put  into  a  partial  or  complete  hypnosis.  Sugges- 
tions and  directions  as  to  cure  are  then  made,  which  the  patient  on  coming 
out  of  his  hypnosis  follows.  This  method  of  treatment  is  uncertain  and 
difficult  and  is  of  use  only  in  a  narrow  field.  It  has  been  practically 
abandoned,  though  occasionally  its  use  gives  brilliant  results,  mainly  in 
hysterical  conditions,  morbid  habits  of  not  long  standing,  and  in  the 
minor  psychoses.  It  is  more  effective  in  the  younger  subjects.  It  is 
of  no  use  in  the  serious  psychoses.     (See  Hypnotism.) 

Suggestion  with  minor  hypnosis  is  only  a  modification  of  the  preceding 
method.  Here  the  patient  is  simply  persuaded  into  a  quiet,  receptive 
mood  or  into  a  slight  degree  of  hypnotic  trance,  which  is  oftener  really 
only  a  slightly  somnolent  state.  Then  suggestions  are  patiently  and 
insistently  repeated.  This  method  is  more  simple  and  on  the  whole 
more  useful  than  the  first.  It  has  to  be  repeated  perhaps  as  often  as  a 
dozen  times  before  the  desired  impression  is  secured.  But  it  is  fairly 
efficient  in  the  pychasthenic,  more  particularly  those  with  fixed  ideas, 
morbid  fears,  attention  pains  and  morbid  melancholic  moods.  The 
treatment  is  most  useful  here  also  in  cases  that  are  not  of  very  long  dura- 
tion. It  deserves  a  permanent  place  in  neurological  therapeutics,  but 
it  can  only  be  applied  by  those  who  have  a  thorough  knowledge  of  the 
patient,  of  the  disease  and,  I  may  add,  of  themselves.  It  requires  a 
steady  and  forceful  and  confident  personality.  Formally  and  strictly 
applied,  it  has  not  a  wide  field.  In  a  simpler  and  common-sense  way, 
however,  the  method  can  be  used  by  any  physician,  and  is  used,  no  doubt, 
all  the  time,  for  it  really  consists  in  giving  the  patient  the  vital  sense  of 
proportion  in  his  judgment  of  things.  In  many  patients  the  harmful 
thoughts  are  not  entirely  subconscious.  The  patient  knows  them,  but 
has  not  quite  recognized  their  importance  and  the  need  of  treating  them 
sanely  and  definitely  and  of  putting  them  in  their  right  relation. 

The  method  of  psychic  analysis  and  reintegration.  This  is  also  called 
the  method  of  Freud.  It  cannot  be  described  in  detail  here.  We  assume 
that  many  of  the  morbid  mental  states  and  bodily  perversions  are  de- 
pendent on  the  presence  of  a  pernicious  and  perhaps  long-forgotten  sub- 
conscious activity. 

Below  the  field  of  ordinary  conscious  processes  there  is  memory  of 
some  earlier  event  acting,  unknown  to  the  patient,  upon  his  conscious 
mental  states  and  inducing  in  him  certain  morbid  ideas  or  emotional 
moods  which  cause  his  sickness.  The  operator,  by  studying  and  ques- 
tioning, by  learning  of  his  dreams,  his  ''running  associations,"  by  telling 
him  to  empty  himself  of  his  troubles  in  a  kind  of  "mental  catharsis," 
brings  into  consciousness  certain  subconscious  states  which  relate  to 
events  of  his  past.     Perhaps  also  he  finds  that  this  lurking  idea  or 


72  DISEASES    OF    THE    NERVOUS    SYSTEM 

emotional  state  is  doing  mischief.  He  then  confronts  the  patient  with 
the  facts,  shows  him  what  is  the  real  cause  of  his  obsession,  persuades 
him  of  its  unreasonableness  or  accustoms  him  to  look  upon  it  in  a  normal 
way.  In  other  words,  he  brings  the  supposed  subconscious  cause  of 
the  trouble  into  consciousness,  readjusts  associations,  and  enables  the 
patient  to  fight  his  trouble  in  the  open. 

It  is  further  claimed  by  the  psycho-analyst  that  the  symptoms  from 
which  the  patient  is  suffering,  the  spasm,  the  obsession,  the  morbid  fear, 
are  really  the  expression  of  a  subconscious  desire  or  of  unsatisfied  in- 
fantile instincts,  usually  of  a  sexual  origin.  My  views  as  to  the  merits 
of  this  doctrine  are  given  in  the  chapter  on  psycho-neuroses. 

The  Method  of  Re-education. — This  may  be  called  also  the  method 
of  ''therapeutic  talk."  It  is  known  as  the  method  of  Du  Bois.  It  is 
really  an  application  of  the  principles  of  suggestion  and  of  readjustment, 
or  re-education,  used  in  the  preceding  methods.  The  patient  has  his 
condition  explained  to  him,  the  aims  of  his  physician  are  placed  before 
him,  the  reasonableness  of  his  cure,  the  unreasonableness  of  his  mental 
state  and  of  his  point  of  view  are  persistently  argued  over.  The  patient 
is  sometimes  persuaded,  sometimes  bullied  into  health.  All  this  is  done, 
however,  after  first  isolating  the  patient  from  everyone  and  clearing  the 
ground  entirely  of  exogenous  irritation.  The  doctor,  with  the  nurse,  a 
necessary  adjunct,  has  the  field  entirely  to  himself.  Obedience  is  en- 
joined. It  is,  in  fact,  a  rest  and  isolation  cure,  combined  with  forceful 
presentations  of  the  reasonableness  and  possibilities  of  cure.  No  medi- 
cines are  given,  as  a  rule.  This  is  a  method  now  having  much  vogue, 
but  it  is  only  a  modification  of  the  Weir  Mitchell  cure,  in  which  the  'psyche 
receives  rather  more  dominantly  the  attention  of  the  physician. 

In  estimating  the  value  of  these  cures  it  must  be  remembered  that 
they  are  useful  practically  only  in  the  psychasthenic  and  neurasthenic 
groups  of  patients.  The  mild  recurrent  melancholias  so  often  mistaken 
for  neurasthenia  get  well  anyway.  The  melancholia  of  involution  is 
little  affected  by  these  methods,  nor  are  the  major  psychoses,  if  we  ex- 
cept perhaps  paranoia  and  early  phases  of  such  types  of  dementia  prsecox 
as  are  largely  of  psychogenic  origin.  The  early  and  abortive  types  of  the 
anxiety  psychosis  may  also  be  affected. 

Empirical  Psychotherapy. — Therapeutic  results  are  obtained  by  man- 
datory methods,  by  the  method  of  extravagant  promise  or  absolute  assur- 
ance. These  are  the  methods  of  the  parent  and  guardian  and  of  the 
charlatan  and  patent  medicine  label.  Their  success  is  more  than  counter- 
balanced by  the  evil  done  by  inconsiderate  assurance  in  improper  cases, 
and  by  misleading  persons  to  the  use  of  measures  not  in  the  least  indi- 
cated by  their  condition. 

The  employment   of  psychotherapy  in   conjunction   with  religious 


HYGIENE,    PROPHYLAXIS,    TREATMENT  73 

work  has  recently  been  advocated  and  in  some  cities  successfully  carried 
out.  A  general  indorsement  of  this  union  of  medical  and  ecclesiastical 
work  cannot  be  given,  and  its  usefulness  must  have  very  definite  limita- 
tions. Still,  under  very  rigid  control,  it  may  prove  an  effective  measure 
and  be  especially  useful  in  counteracting  the,  on  the  whole,  bad  influence 
of  various  types  and  schools  of  ''healers."  One  measure  cannot  cure  all 
diseases  or  even  all  of  one  kind  of  disease,  and  the  exploitation  of  infallible 
cures  works  an  injury  to  society  in  the  end. 

Psychotherapy  by  Emotional  Shock. — This  is  seen  typically  in  the 
exhortations  of  religious  healers  and  the  dramatic  methods  of  charlatans. 

Philosophic  Psychotherapy. — Most  successful  results  are  obtained 
among  the  always  large  number  of  suggestible  and  credulous  minds  by 
instillating  a  certain  formula,  squared  by  which  their  symptoms  must 
cease  and  the  disease  disappear.  This  is  the  method  of  the  Doctrinaire, 
or  Philosopher,  or  Apostle.  For  example,  it  is  asserted  that  God  is  good, 
God  is  all,  therefore  there  can  be  no  evil  in  you.  Sickness  is  an  evil, 
therefore  it  cannot  exist.  Therefore  you  cannot  be  sick.  You  are  well. 
This  doctrine  ingeniously  and  eloquently  poured  into  simple  ears  gradu- 
ally gains  conviction,  the  patient  receives  assurance,  the  attention  is 
distracted  from  morbid  symptoms  and  the  patient  gets  well — sometimes. 
The  doctrine  applied  to  many  thousands  always  reaches  some  who  only 
need  this  distraction  of  attention  from  themselves.  They  ignore  symp- 
toms, and  gradually  their  consciousness  gets  less  sensitive  to  them.  They 
harden  their  sensorium,  and  though  they  have  conditions  which  would 
make  some  sensitive  souls  feel  distressed,  these  conditions  do  not  arouse 
their  attention  which  is  complacently  and  wisely  directed  elsewhere. 

The  only  objection  to  this  method  of  therapeutics  is  that  its  funda- 
mental propositions  are  unproven,  and  its  general  application  to  surgery, 
infectious  and  organic  disease  is  disastrous.  But  the  philosophy  of  at- 
tention diversion  to  the  healthy  and  holy  side  of  life  is  wise  and  is  indeed 
used  by  all  physicians  and  in  every  form  of  scientific  psychotherapeutics. 

An  essential  thing  in  all  forms  of  systematic  psychotherapy  is  to 
have  the  patient  on  the  proper  stage.  He  or  she  must  be  removed 
from  all  influences  but  those  of  the  doctor  and  his  attendants.  The 
atmosphere  must  be  such  that  only  his  personality  and  views  and  counsels 
affect  the  patient.  Then  the  work  must  be  kept  up  for  at  least  a  few 
weeks  and  often  longer.  With  this  environment,  the  results  are  reason- 
ably certain  in  proper  cases.  But  without  it,  there  is  only  a  chance 
that  the  wisest  counsel  prevail. 

Then  the  physician  himself  must  be  suited  to  the  kind  of  work. 
He  need  not  have  a  commanding  personality,  but  he  must  be  simple  and 
impressive  and  sincere,  and  he  must  have  no  unpleasant  personal  habits. 


74  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  nurse,  if  there  is  one,  must  equally  be  a  person  of  tact  and 
experience,  good  personality  and  able  to  co-operate. 

It  can  be  seen  that  the  systematic  application  of  psychotherapeutics, 
at  its  best,  is  not  possible  for  all,  and  is  not  suitable  for  most.  Its 
unsystematic  or  rather  informal  use  will  always  be  a  part  of  the  equip- 
ment of  the  wise  physician.  It  makes  it  all  the  more  imperative  that 
physicians  be  good  as  well  as  wise. 


CHAPTER  VII 
DISEASES  OF  THE  PERIPHERAL  NERVES 

Introduction. — The  peripheral  nervous  system  consists  (1)  of  twelve 
pairs  of  cranial  and  thirty-one  pairs  of  spinal  nerves,  with  their  root 
ganglia  and  terminal  sense  organs;  (2)  and  of  the  sympathetic  nervous 
system  including  the  autonomic  portion  of  Langley.  The  peripheral 
nervous  system,  therefore,  to  use  the  language  of  modern  anatomy, 
is  composed  of  peripheral  motor  neurons,  peripheral  sensory  neurons, 
and  peripheral  ganglionic  neurons  (Minot). 


GENERAL  PATHOLOGY 

Hyperaemia  and  Anaemia.— Under  the  head  of  hypersemia  and 
anaemia  there  occur  types  of  nerve  irritation,  leading  to  different  forms 
of  neuralgia,  parsesthesia  and  motor  weakness  or  irritation.     Hypersemia 


Fig.  33. — Showing  the  cells  of  origin  of  the  motor  nerves  in  the  anterior  horns  of 
the  spinal  cord,  and  the  cells  of  origin  of  the  sensory  nerves  in  the  posterior  spinal 
ganglia.     {Van  Gehuchten.) 

and  anaemia  are,  however,  secondary  conditions  and  are  rarely  recog- 
nized clinically.  It  cannot  always  be  determined  whether  an  irritated 
nerve  is  congested  or  anaemic,  or  whether  the  central  part  of  the  nervous 
system  is  not  mainly  at  fault. 

Angina  of  the  Nerves. — ^In  arterio-sclerotic  conditions  of  the  blood- 
vessels of  the  posterior  ganglia  and  nerves  there  occur  spasmodic  closures 

75 


76  DISEASES    OF   THE    NERVOUS    SYSTEM 

of  the  vessels  or,  in  other  words,  anginal  attacks,  which  cause  severe 
neuralgic  pains.  The  pathology  of  this  condition  will  be  referred  to 
later. 

Inflammation  of  Nerves — Neuritis. — There  are  two  principal  forms  of 
neuritis:  (1)  Interstitial  and  perineuritis.  (2)  Diffuse  neuritis  with 
parenchymatous  degeneration  or  parenchymatous  neuritis.  The  two 
forms  may  be  acute  or  chronic. 

In  the  first  type  there  is  hypersemia,  with  sometimes  extravasation 
of  blood.  An  exudation  occurs  into  the  fibrous  framework  of  the  nerve, 
with  migration  of  leukocytes.  The  inflammation  may  become  suppurative 
or  gangrenous.  If  severe,  it  destroys  the  nerve-fibres;  but  oftenest  the 
axis-cylinders  are  not  destroyed,  and  recovery  takes  place. 

In  mild  grades  of  perineuritis,  such  as  occurs  in  sciatica,  there  is  peri- 
neuritic  exudation,  a  kind  of  serous  inflammation  with  not  much  cellular 
proliferation.  This  perineuritis  is  probably  the  main  factor  in  the 
typical  neuralgias  like  sciatica  neuralgia. 

Chronic  interstitial  neuritis  and  perineuritis  are  accompanied  with 
hyperplasia  of  the  connective  tissue,  compression  and  more  or  less  destruc- 
tion of  the  nerve  (Fig.  34).  It  may  ascend  or  descend,  and  it  is 
called,  accordingly,  ascending,  descending,  or  migrating  neuritis.  It  may 
affect  only  certain  segments  of  the  nerve,  when  it  is  called  segmental 
neuritis  or  disseminated  neuritis.  Tuberculous  and  syphilitic  neuritis  are 
of  the  chronic  interstitial  or  diffuse  type.  These  latter  forms  rarely  in- 
volve peripheral  nerves,  but  rather  the  intracranial  parts  of  the  cranial 
nerves  and  the  spinal  nerve-roots  in  meningeal  tuberculosis  or  syphilis. 
A  syphilitic  peripheral  multiple  neuritis  is,  however,  thought  to  occur 
sometimes.  Leprous  neuritis  is  a  very  typical  form  of  proliferating 
chronic  perineuritis.  Cancerous  neuritis  sometimes  occurs  and  it  is  of 
the  diffuse  type,  though  sometimes  an  actual  cancerous  process  invades 
the  nerve. 

The  second  type  is  called  parenchymatous  or  degenerative  neuritis 
and  this  process  of  degeneration  is  the  dominant  one,  so  that  the  changes 
can  be  best  described  under  the  head  of  degeneration  of  nerves. 

Degeneration  of  Nerves. — This  is  a  process  in  which  the  nerve-fibres 
gradually  die;  the  myelin  sheath  and  axis-cylinder  disappear,  leaving 
only  a  strand  of  connective  tissue. 

There  are  three  forms  of  nerve  degeneration:  (1)  primary;  (2)  sec- 
ondary;  (3)   neuritic   or  toxic. 

1 .  The  primary  form  is  rare,  slight  in  extent,  and  of  little  clinical  sig- 
nificance. In  it  there  is  simply  a  gradual  wasting  and  disappearance  of 
the  axis-cylinder  and  myelin  sheath.  It  occurs  in  old  age,  wasting  dis- 
eases and  as  part  of  locomotor  ataxia. 

2.  Secondary  degeneration  or  Wallerian  degeneration.     This  form 


DISEASES    OF   THE    PERIPHERAL   NERVES 


77 


occurs  when  the  nerve  is  cut  across   or   compressed,  or  destroyed  by 
inflammation,  neoplasms  or  injuries. 

The  essential  part  of  the  nerve-fibre,  the  axis-cylinder,  is  simply 
a  prolongation  of  the  process  of  a  nerve-cell.  Its  next  essential  part  is  the 
myelin  sheath.  This  is  of  epiblastic  origin  and  consists  of  a  hollow 
cylinder  inclosed  in  a  thin  membrane  and  containing  a  fatty  substance. 
In  degenerative  processes  of  peripheral  nerves  the  medullary  sheath 
is  first  affected,  then  the  axis-cylinder,  least  and  last  the  neurilemma. 


Fig.  .34. — Interstitial  neuritis. 


The  myelin  becomes  turbid,  splits  up  into  fragments  and  droplets.  The 
axis-cylinder  also  breaks  up  into  fragments  or  swells  up  and  becomes 
liquefied.  Extravasated  leukocytes  pick  up  the  products  of  disintegra- 
tion and  form  fat-granule  cells.  The  neurilemma  and  its  nuclei  usually 
remain  intact.  The  nerve  during  this  time  shrinks  in  volume  and  looks 
grayish  and  translucent,  or  grayish-red.  The  nerve  finally  becomes  only 
a  fibrous  cord.  Changes  can  be  seen  in  the  nerve  within  forty-eight 
hours,  and  by  this  time  its  irritability,  which  was  first  slightly  increased, 


78  DISEASES    OF    THE    NERVOUS    SYSTEM 

is  lost.  In  about  two  weeks  the  disintegration  of  the  myehn  sheath  and 
axis  is  practically  complete.  The  peripheral  end  of  the  cut  nerve 
shows  a  loss  of  nearly  but  not  quite  all  the  fibres  as  far  as  its  termination. 
In  the  central  end,  the  degeneration  ascends  at  first  only  to  the  first  or 
second  node  of  Ranvier.  Very  soon,  however,  a  change  occurs  in  the  cell 
from  which  the  fibre  springs.  This  change  is  called  the  reaction  at  a 
distance,  or  degeneration  of  Nissl.  Thus  when  the  neuraxon  is  injured 
the  whole  neuron  suffers,  but  the  peripheral  end  far  the  most. 

When  a  section  is  made  between  the  spinal  ganglia  and  the  cord,  the 
fibres  all  degenerate  toward  the  cord,  and  even  within  it,  but  the  peripheral 
fibres  do  not  degenerate.  Hence  the  spinal  ganglia  are  the  trophic  cen- 
tres of  the  sensory  nerves  (see  Fig.  35). 

Degeneration  occurs  in  the  motor  nerves,  also,  when  the  cells  of 
the  anterior  horns  are  destroyed.     Hence  these  cells  are  the  trophic 


S.G.  ^ 

Fig.  35. — Showing  effects  of  section  of  mixed  nerves  and  sensory  root.  PMN.,  Sec- 
tion through  mixed  nerve;  MR.,  motor  root;  S.R.,  sensory  root;  S.G.,  spinal  ganglion; 
Pc,  peripheral  ganglion. 

centres  for  all  motor  nerves.  The  process  of  degeneration  takes  place 
at  about  the  same  time  throughout  the  whole  length  of  the  nerve.  The 
motor  end-plates  in  the  muscles  are  affected  a  little  the  earliest.  About 
the  cut  end,  little  bulbous  tumors  may  develop,  which  contain  numerous 
nerve  fibrils  and  connective  tissue.  The  general  law  is  that  nerves  de- 
generate in  the  direction  in  which  they  carry  impulses,  but  this  is  not  the 
whole  case,  as  has  been  just  described.  If  the  injury  to  the  nerve 
is  permanent,  a  slow  decay  affects  the  whole  neuron.  Supposing  for  ex- 
ample a  motor  nerve  is  injured  or  inflamed  at  the  point  D.  Immediately 
a  degeneration  takes  place  along  the  parts  below  to  T,  and  in  a  few  days  a 
slight  degeneration  takes  place  in  the  cell-body  C  (see  Fig.  36) . 

Within  the  central  nervous  system  degeneration  also  occurs  mainly  in 
the  direction  of  the  nerve  impulse.  The  axis-cylinder  is  first  affected. 
There  is  sometimes  a  preliminary  swelling  or  hypertrophy  of  this  axis- 
cylinder.  Degeneration  with  calcification  of  the  nerve-fibres  sometimes 
occurs.  In  associative  or  commissural  fibres  the  degeneration  extends 
only  part  of  the  length  of  the  nerve. 

3.  Neuritic  and  toxic  nerve  degeneration.  This  form  occurs  in  con- 
nection with  neuritis,  and  will  be  described  under  that  head.     Its  chief 


DISEASES    OF    THE    PERIPHERAL   NERVES  79 

characteristics  are  that  the  degeneration  attacks  the  nerve  in  segments, 
that  the  axis-cyHnders  are  not  so  much  affected,  and  the  myehn  breaks 
up  into  small  fatty  droplets  instead  of  into  large  masses.  The  same 
general  laws  apply  to  it  as  to  Wallerian  degeneration. 

Degenerative  processes  in  the  non-medullated  nervous  fibres  have 
been  observed  in  the  fine  fibres  of  the  cornea  and  in  the  submucous  and 
mesenteric  plexuses  of  the  alimentary  tract. 

Regeneration  of  nerves  is  a  process  that  usually  follows  degeneration. 
It  occurs  only  in  peripheral  nerves — very  little,  if  at  all,  in  the  nerves 
of  the  central  nervous  system  of  mammals.  It  is  an  unique  process,  in 
that  the  nerve  is  the  only  specialized  tissue  that  can  grow  again  after 
being  destroyed.  Regeneration  occurs  whenever  the  trophic  centres  are 
healthy,  when  the  mechanical  obstacles  to  a  union  of  the  divided  fibre 


Fig.  36. 

are  not  too  great,  and  when  the  peripheral  nerve  is  not  too  completely 
atrophied.  It  occurs  most  quickly,  therefore,  when  the  cut  ends  are 
carefully  apposed  and  when  the  separation  has  not  lasted  for  a  long  time, 
i.e.,  for  years.  It  progresses  always  from  the  central  end  toward  the  per- 
iphery. The  fibres  of  the  central  stump  grow  out  into  the  degenerated 
peripheral  fibre.  Union  by  first  intention  or  second  intention  never 
occurs.  Human  nerves  cannot  be  made  to  unite  physiologically,  but 
only  anatomically. 

Regeneration  may  be  complete  in  a  few  months  in  short  nerves. 
In  the  sciatic  it  may  take  one  or  two  years.  When  regeneration  takes 
place,  the  axis-cylinders  of  the  central  stump  swell  and  divide  into  a 
number  of  new  cylinders  which  pierce  or  creep  around  the  intervening 
tissue,  enter  in  bundles  the  peripheral  nerve,  and  become  inclosed  in  new 
myelin  sheaths  and  neurilemma. 

GENERAL  SYMPTOMS 

The  dominant  symptoms  occurring  in  the  distribution  of  the  peripheral 
nerves  are  paralysis  and  atrophy  of  muscles  in  a  greater  or  less  degree  to- 
gether with  sensory  disorders.  But  since  the  mixed  nerve  carries  with  it 
some  vasomotor  and  secretory  fibres,  there  may  also  be  congestion,  oedema, 
and  dryness  or  sweating  of  the  skin.     When  a  peripheral  motor  neuron  is 


80  DISEASES    OF    THE    NERVOUS    SYSTEM 

damaged  only  to  a  moderate  extent  or  is  irritated  by  any  agent,  twitch- 
ings  of  the  muscle  (myokinia)  may  occur.  But  direct  irritation  of  the 
peripheral  motor  nerve  does  not  cause  spasms. 

NEURITIS  AND   MULTIPLE  NEURITIS 

The  common  disorder  of  peripheral  nerves  is  inflammation  or  neuritis. 
When  this  inflammation  affects  many  nerves  it  is  called  multiple  or  poly- 
neuritis. When  it  affects  one  nerve  or  nerve  group  it  is  called  mono- 
neuritis. The  terms  plexus  neuritis  and  root  neuritis  may  indicate  more 
specifically  the  location  of  the  disease. 

The  following  table  shows  the  classification  on  an  etiological  basis  of 
the  different  types  of  neuritis: 

Mono-neuritis 

Traumatic  neuritis 

Reflex  joint  neuritis 

Occupation  neuritis 

Rheumatic,  infectious  and  toxic  neuritis. 
Multiple  neuritis 

Infectious  neuritis 

Beri-beri,  diphtheria,  sepsis 

Toxic  neuritis 

(a)  Endogenous,  diabetic,  cachectic,  puerperal  and  senile,  etc. 

(b)  Exogenous,  alcohol,  CO,  CS2  sulphinal,  lead,  arsenic,  mercury,  etc. 

MULTIPLE  NEURITIS— POLYNEURITIS 

Multiple  neuritis  has  been  divided  into  many  types  in  accordance 
with  the  cause,  the  location  of  the  process,  and  the  complications. 

1.  The  common  type  is  a  motor-sensory  one  involving  all  four  ex- 
tremities and  due  oftenest  to  alcohol.  Here  the  paralysis  is  a  dominant 
feature. 

2.  Sometimes  the  sensory  and  ataxic  symptoms  are  dominant, 
forming  a  sensori-ataxic  type  which  is  quite  rare  and  is  due  more  often 
to  infections  and  other  poisons  than  alcohol. 

3.  A  pernicious  and  hemorrhagic  type  exists  but  is  also  rare.  It  is 
due  to  overwhelming  toxaemia. 

There  is  also  a  pure  motor  neuronitis,  multiple  in  character,  due 
oftenest  to  lead;  and  there  is  a  degenerative  neuritis  of  the  sensory 
neurons,  especially  noted  in  diabetes. 

It  seems  best  not  to  have  too  many  kinds  of  multiple  neuritis,  and 
in  fact  the  motor-sensory  type  is  the  common  and  real  disease;  the  others 
are  terminal  conditions,  complications  or  sequelae. 

The  Sensory-motor  Type  of  Multiple  Neuritis  (Alcoholic  Paralysis, 
Arsenical  Paralysis,  Diphtheritic  Paralysis). — -This  is  the  common  form 


DISEASES    OF    THE    PERIPHERAL    NERVES  81 

of  the  disease,  making  up  fully  90  per  cent,  of  all  cases  seen  in  the 
country.  While  sensory  and  other  symptoms  always  accompany  this 
type,  it  is  the  paralysis  and  atrophy  of  muscles  which  are  the  leading  and 
chronic  conditions.  It  is  a  malady  coming  on  acutely,  running  a  sub- 
acute or  chronic  course,  rarely  fatal,  and  characterized  by  weakness  or 
paralysis  of  all  four  extremities,  associated  with  atrophy,  pain,  tenderness 
and  various  vasomotor,  secretory  and  trophic  disturbances.  It  is  a  dis- 
ease pre-eminently  due  to  poisons  and  infections,  alcohol  being  far  the 
commonest  factor. 

It  occurs  oftener  in  the  female,  owing  to  the  fact  that  women  are 
more  anaphylactic  to  alcohol  than  men,  and  perhaps  also  because  of  the 
predisposing  influence  of  tea-drinking. 

Multiple  neuritis  is  essentially  a  disease  of  early  adult  life.  Almost 
all  cases  occur  between  adolescence  and  the  period  of  degenerative 
changes,  twenty  to  forty-five.  Young  children  are  very  rarely  subject  to 
it,  but  cases  have  been  reported  occurring  in  children  at  the  age  of  seven, 
nine,  ten  and  fourteen.  A  few  cases  have  occurred  in  persons  over 
sixty,  but  they  are  only  a  little  less  susceptible  than  children.  It  occa- 
sionally occurs  as  an  epidemic  and  is  then  due  to  some  infection.  Beri- 
beri is  a  particular  type  of  toxic  multiple  neuritis. 

The  sporadic  forms  of  polyneuritis  from  alcohol  and  various  poisons 
and  infections  occur  without  much  reference  to  a  seasonal  influence. 
Probably  more  cases  occur  in  spring  and  fall,  owing  to  sudden  changes 
in  temperature.  Epidemic  influence  like  that  causing  cerebrospinal 
meningitis  may  increase  the  number  of  cases  of  multiple  neuritis.  Prac- 
tically, in  this  country,  the  question  of  drink  settles  the  question  of  the 
distribution  of  polyneuritis.  It  is  rare  in  the  temperate  rural  districts 
and  smaller  towns,  and  much  rarer  in  native  Americans  than  in 
foreigners. 

Sexual  excesses,  exposure  to  cold  and  wet,  insufficient  diet,  excessive 
tea-drinking  and  the  presence  of  tuberculosis  predispose  to  the  disease. 
The  same  neuropathic  tendency  leading  persons  to  excesses  in  alcohol, 
tea  and  to  suicidal  indulgence  in  arsenic  is  of  some  moment  in  leading  to 
the  development  of  neuritis. 

The  list  of  the  special  and  exciting  causes  is  long  and  includes  nearly 
all  infectious  fevers,  many  chemical  and  autochthonous  poisons.  The 
common  infections  are  diphtheria,  puerperal  and  other  septic  fevers, 
and  endemic  infections  of  unknown  origin.  Nearly  every  infectious  fever 
and  possibly  malaria  may  be  added  to  the  list. 

Of  chemical  poisons  alcohol  heads  the  list,  causing  over  two-thirds  of 
the  adult  cases.  Next  come  arsenic,  lead  and  phosphorus,  mercury, 
copper  and  trional.  Wood  alcohol  is  extremely  poisonous,  and  may 
promptly  cause  a  multiple  neuritis.     It  has,  however,  a  special  tendency 


82  DISEASES    OF    THE    NERVOUS    SYSTEM 

to  cause  optic  neuritis  and  blindness.  Even  so  small  an  amount  as  3  oz. 
has  caused  blindness  and  5  oz.  blindness  and  death. 

Among  the  autochthonous  poisons,  diabetes  and  the  metabolic 
products  resulting  from  starvation  and  cachexia  lead  to  multiple  neuritis. 

Among  the  foregoing  causes,  arsenic  and  diabetes  produce  more  often 
decided  sensory  symptoms.  One  attack  does  not  confer  immunity,  but 
it  generally  compels  prudence  so  that  second  attacks  are  rare. 

Symptoms. — The  disease  often  begins  with  prodromata  lasting 
several  weeks.  The  patient  suffers  from  numbness,  slight  pains,  and 
weakness  affecting  especially  the  lower  extremities.  Sometimes  a  pe- 
culiar condition  of  mental  confusion  and  weakness  precedes  the  attack. 
Usually  the  symptoms  come  on  rather  suddenly.  The  patient  suffers 
from  pains  and  tenderness  in  the  legs  and  feet,  and  is  obliged  to  go  to  bed. 
There  may  be  a  fever  for  a  day  or  two,  the  temperature  rising  to  102°  or 
even  104°F.,  but  this  is  not  the  rule.  The  pains  and  weakness  increase. 
The  muscles  and  nerves  are  very  tender.  The  fingers,  hands  and  arms 
are  often  similarly  but  less  affected.  At  the  same  time  the  skin  becomes 
reddened  or  slightly  oedematous.  The  muscles  of  the  legs  grow  weak, 
and  in  a  day  or  two  the  patient  is  unable  to  stand.  In  a  week  or  two  there 
may  be  a  complete  loss  of  power  in  the  anterior  tibial  muscles  and  a  lesser 
degree  of  paralysis  in  the  extensors  of  the  hand  (Fig.  37).  Nearly  all  of 
the  leg  and  forearm  muscles  become  eventually  involved.  Atrophy  sets 
in  at  the  same  time  and  very  severe  pains  are  present.  The  motor  cranial 
nerves  are  in  rare  cases  affected,  and  paralysis  of  the  facial  or  of  the  third, 
fourth  or  sixth  nerve  has  been  seen.  When  the  disease  is  fully  de- 
veloped, which  is  within  a  fortnight,  there  is  paraplegia  with  foot-drop, 
some  degree  of  wrist-drop,  muscular  atrophy,  and  slight  oedema,  espe- 
cially of  the  feet.  The  skin  reflexes  are  often,  the  knee-jerk  and  elbow-jerk 
usually,  lost.  There  is  some  tactile  anaesthesia,  often  with  hyperalgesia. 
Temperature  and  pain  sense  are  later  lessened  and  slowed  in  trans- 
mission. The  anaesthesia  occurs  in  patches  or  diffusely.  Muscle  and 
articular  sense  are  lost  in  the  sensory  or  pseudotabetic  form,  and  are 
usually  somewhat  involved  in  the  ordinary  paralytic  form.  Pain  and 
sensitiveness    continue. 

The  nerves  lose  their  irritability  and  the  muscles  show  degeneration 
reaction,  partial  or  complete,  the  characteristic  being  a  great  variability 
of  reaction  over  different  groups  of  nerves  and  at  different  stages  of  the 
disease,  and  an  early  loss  of  faradic  and  lessening  of  galvanic  irritability. 
There  is  sometimes  retinal  hypersemia  and  even  optic  neuritis.  Of  the 
visceral  nerves,  the  vagus  seems  oftenest  to  show  signs  of  involvement, 
with  rapid  pulse  and  disturbances  of  respiration.  In  rare  cases  the 
phrenic  nerve  is  involved.  Three  such  cases  were  observed  in  the  wards 
of  Bellevue  Hospital  in  two  years.     The  sphincters  are  rarely  affected 


DISEASES    or    THE    PERIPHERAL    NERVES 


S3 


and  then  only  for  a  few  days.     In  such  cases  there  is,  perhaps,  involve- 
ment of  the  cord  or  of  the  abdominal  and  pelvic  splanchnics. 

In  alcoholic  and  occasionally  in  other  forms  of  nemitis,  mental 
symptoms,  such  as  a  low,  muttering  delirium,  are  very  often  present,  and 
occasionally  a  well-marked  confusional  insanity  develops.  (Korsakoff's 
psychosis.) 

The  disease  usually  reaches  its  height  in  a  week  or  two  and  then 
starts  on  a  chronic  course;  but  it  sometimes  happens  that  exacerbations 
occur,  or  that  a  paralysis  and  atrophy 
progress  for  several  weeks  before  re- 
gression begins.  In  alcoholic  cases 
there  is  often  great  general  prostration; 
the  patients  lie  for  several  weeks  in  a 
delirious  condition,  and  finally  develop 
pneumonia  and  die. 

In  diphtheritic  neuritis  some  of  the 
eye  and  throat  muscles  (ciliary  muscle 
and  soft  palate)  are  involved,  while  the 
extremities  are  usually  but  slightly  or 
temporarily  affected  and  the  sensory 
symptoms  are  few. 

Some  further  details  should  be 
added. 

Motor  Symytoms. — The  character- 
istic paralysis  of  multiple  neuritis  is  a 
quadruplegia,  all  four  extremities  being 
involved.  The  special  characteristic  is 
the  foot-drop,  which  is  indicative  of 
alcoholic  neuritis  just  as  wrist-drop  is 
of  lead  palsy.  The  paralysis  is  typi- 
cally a  peripheral  one.  It  affects  the 
feet  and  legs,  hands  and  forearms.  It 
usually  involves  the  anterior  tibial 
muscles  more  than  the  calf  muscles, 
but  sometimes  the  reverse  occurs.  The 
muscles  become  wasted  and  flabby. 
They  soon  lose,  in  bad  cases,  all  reaction  to  faradism,  and  they  require  a 
strong  galvanic  current  to  produce  a  contraction.  In  anterior  poliomye- 
litis, on  the  other  hand,  the  diminution  in  galvanic  irritability  comes  on 
only  after  weeks  or  months.  Hence  an  early  loss  of  galvanic  as  well  as 
faradic  reaction  is  an  important  sign  of  neuritis.  As  the  nerve  and  muscle 
recuperate,  the  galvanic  irritability  increases.  After  a  time,  if  the  par- 
alysis is  great,  contractures  occur.     The  feet  are  extended,  the  wasted 


Fig.  37. — Alcoholic  mutiple  neuritis 
with  foot- drop  and  wrist-drop. 


84  DISEASES    OF    THE    NERVOUS    SYSTEM 

legs  are  flexed  on  the  thighs  and  are  almost  immovable,  and  the  patient's 
condition  is  one  of  pitiable  helplessness. 

Sensory  Symptoms. — Numbness,  hypersesthesia,  severe  pains  (dull 
and  sharp),  burning  sensations,  great  tenderness  all  occur  and  are 
very  marked  symptoms.  They  are  felt  mostly  in  the  feet,  legs  and  hands. 
Hypersesthesia  is  usually  followed  by  anaesthesia  to  touch  and  somewhat 
to  pain  and  temperature.  The  transmission  of  these  latter  two  sensations 
is  delayed.  The  angesthesia  sometimes  occurs  in  patches,  at  other  times 
diffusely  over  foot,  leg  and  hand.  Muscular  and  articular  anaesthesia  are 
common,  and  in  the  sensory  form  are  the  dominant  symptom,  causing  an 
ataxia  of  gait  and  station.  The  other  special  senses  are  not  affected  ex- 
cept in  rare  cases  in  which  there  is  optic  neuritis. 

Vasomotor  and  Trophic  Symptoms. — There  is  often  oedema,  some- 
times redness  of  the  skin;  occasionally  the  epidermis  of  the  soles  and 
palms  peels  off.  Glossy  skin  and  profuse  perspiration  are  rare.  Erup- 
tions and  ulcers  do  not  occur. 

Mental  Symptoms. — The  most  common  mental  disturbance  is  that  so 
often  seen  in  acute  alcoholism,  viz.,  clouded  consciousness  and  a  low 
muttering  delirium.  This  is  associated  with  great  general  vital  depres- 
sion. If  a  true  insanity  develops  it  is,  as  a  rule,  of  the  type  known  as 
Korsakoff's  psychosis.  The  characteristic  symptoms  are  a  curious  de- 
gree of  forgetfulness  and  disorientation,  together  with  many  and  varying 
hallucinations  and  delusions  rapidly  succeeding  each  other.  These  often 
relate  to  the  pains  and  parsesthesia  from  which  the  subjects  suffer.  They 
think  that  there  are  gloves  on  their  hands  or  that  something  is  on  their 
feet.  They  often  think  that  they  have  been  out  walking  or  riding.  They 
are  talkative,  incoherent  and  sleepless. 

Organic  Centres. — The  bladder  is  occasionally  affected  for  a  short 
time,  the  other  centres  not  at  all.  This  freedom  from  involvement  of  the 
sphincters  is  an  important  characteristic  of  the  disease  in  distinguishing 
it  from  myelitis. 

The  hlood  shows  a  moderate  degree  of  leukocytosis  in  uncomplicated 
cases. 

From  the  foregoing  it  will  be  seen  that  the  dominant  symptoms  are 
parsesthesia,  pains  (burning,  lancinating  and  dull),  muscular  tenderness, 
some  anaesthesia,  paralysis  affecting  especially  the  lower  extremities  and 
causing /oo^-c^rop,  muscular  wasting,  with  degeneration  reactions;  with  no 
involvement  of  the  sphincters;  sometimes  peculiar  mental  disturbances. 

The  sensori-ataxic  or  pseudo-tabetic  type  of  multiple  neuritis  is 
caused  less  often  by  alcohol  and  more  often  relatively  by  diabetes  and  the 
metallic  and  infectious  poisons.  Arsenic  given  medicinally  in  doses  of 
one-sixth  of  a  grain  or  more  may  cause  such  a  neuritis.  Multiple  neuritis 
from  lead  is  not  often  seen  in  painters  who  suffer  only  mainly  from  wrist- 


DISEASES    OF    THE    PERIPHERAL    NERVES  85 

drop,  but  usually  occurs  when  the  poison  is  taken  in  large  doses.  The 
general  course  of  sensory  neuritis  is  much  hke  that  of  the  paralytic  form, 
but  there  is  less  paralysis  and,  on  the  other  hand,  there  are  more  of  the 
burning,  tearing  pains,  a  greater  degree  of  anaesthesia,  with  a  very  decided 
muscular  anaesthesia  causing  symptoms  of  a  subacute  locomotor  ataxia. 
The  paresis,  muscular  wasting,  trophic  changes,  such  as  shedding  of  the 
epidermis  and  the  electrical  reactions,  serve  to  distinguish  the  disease. 
A  facial  paralysis  sometimes  complicates  this  type. 

Endemic  and  Epidemic  Types  (Beri-beri  or  Kakke,  Ignipedites,  Acro- 
dynia,  Malarial  Multiple  Neuritis). — Beri-beri  or  endemic  multiple 
neuritis  is  seen  in  this  country  rarely,  and  only  by  accident.  Beri-beri 
is  the  Indian  name;  kakke,  meaning  "the  leg  disease,"  is  its  Japanese 
name.  Ignipedites  is  a  name  given  by  Indian  physicians  to  probably  the 
same  disease.  French  physicians  gave  the  name  of  "acrodynia"  to  an 
epidemic  disease  which  prevailed  in  France  and  the  Crimea  in  the  early 
part  of  the  last  century.  It  was  probably  multiple  neuritis.  Epidemic 
multiple  neuritis  has  been  observed  in  two  State  hospitals  in  this  country, 
in  Alabama  and  Arkansas.  It  has  also  been  observed  in  epidemics  in 
New  York,  Connecticut  and  Vermont.  The  disease  is  due  mainly  to  a 
monotonous  and  more  or  less  exclusive  diet  of  unpolished  rice.  It  may  be 
produced  also  by  a  monotonous  diet  of  other  starchy  substances,  such  as 
wheat;  over-crowding,  bad  hygienic  conditions,  heat,  moisture  and  ex- 
posure favor  its  development. 

There  are  various  types  of  this  disease,  in  some  of  which  the  neuritic 
symptoms  seem  subordinate  to  those  of  other  organs.  The  forms  de- 
scribed are: 

The  paraplegic  or  dry,  the  dropsical  or  wet,  and  the  mixed  and  very 
acute  forms. 

The  symptoms  generally  resemble  those  of  multiple  neuritis,  as  already 
described,  plus  oedema,  extensive  serous  effusions,  serious  heart  weak- 
ness and  gastro-intestinal  disorders.  I  have  observed  a  case  of  undoubted 
endemic  neuritis  (beri-beri)  which  ran  precisely  like  an  ordinary  multiple 
neuritis.  The  paralysis  affects  especially  the  lower  extremities,  but  in 
beri-beri  there  seems  to  be  an  especial  tendency  also  to  involvement  of 
vasomotor  and  visceral  nerves.  The  disease  runs  a  course  like  other  types 
of  toxic  neuritis.  It  can  be  cured  by  feeding  with  rice  bran,  adding  other 
substantial  food. 

Malarial  Multiple  Neuritis. — It  is  hkely  that  ''malarial"  multiple 
neuritis  is  only  a  form  of  beri-beri  which  is  not  rare  in  some  of  the  islands 
of  the  West  Indies. 

Acute  Pernicious  Multiple  Neuritis — The  Heine-Medin  Disease. — 
There  is  a  form  of  multiple  neuritis  which  comes  on  suddenly,  progresses 
rapidly,  and  causes  death  in  a  few  days  or  weeks.     These  cases  usually 


86 


DISEASES    OF    THE    NERVOUS    SYSTEM 


show  the  ordinarj^  symptoms  of  neuritic  paralysis,  with  final  involvement 
of  the  cardiac  and  respiratory  nerves,  causing  death.  The  neuritis  is 
interstitial  and  hemorrhagic.  The  disease  is  due  to  an  infectious  poison 
which  overwhelms  the  system  before  it  has  time  to  set  up  any  inflammation 
or  organic  change.  In  these  cases  the  anterior-horn  cells  of  the  spinal 
cord  are  also  involved,  and  the  disease  is  one  that  attacks  the  whole 
peripheral  motor  neuron.  It  is  probable  that  Landry's  paralysis  and 
this  severe  form  of  multiple  neuritis  are  due  to  the  same  cause,  and  that 
they  are  allied  to,  if  not  one  phase  of,  acute  anterior  poliomyelitis  forming 
a  part  of  the  Heine-Medin  disease.  This  is  the  name  given  to  the  in- 
fection which  causes  the  above-mentioned  diseases  as  was  as  encephalitis. 
Pathology. — In  multiple  neuritis  the  disease  affects  the  periphery  of 
the  nerves  most,  and  extends  up,  very  rarely  reaching  the  roots.     The 


Fig.  38. — Alcoholic  neuritis  parenchymous  degeneration. 


anterior  tibial  and  musculo-spiral  nerves  on  the  two  sides  are  oftenest  and 
most  diseased.  The  process  when  mild  in  grade  resembles  a  secondary 
degeneration  following  section  of  the  nerve  (Fig.  38).  In  severer  cases 
there  is  evidence  of  interstitial  inflammation  as  well  as  degeneration. 
This  process,  however,  varies  in  degree  at  different  points  of  the  nerve's 
course.  Hence  it  has  been  called  segmental  or  disseminated  neuritis. 
In  some  of  these  cases  and  in  all  acute  pernicious  cases  there  is  still  more 
interstitial  inflammatory  change;  small  hemorrhages  occur,  exudation  takes 
place,  and  collections  of  leukocytes  about  the  vessel  walls  and  among 
the  nerve-fibres  are  seen  (Fig.  39).  The  muscles  supplied  by  the  dis- 
eased nerves  undergo  atrophy.  This  is  usually  simple  and  non-inflamma- 
tory.    But  sometimes  there  is  an  interstitial   myositis  with  exudation 


DISEASES    OF    THE    PERIPHEEAL    NERVES 


87 


compressing  the  fibres  (Senator).  If  the  disease  progresses,  the  nerve- 
fibres  degenerate  and  their  place  is  taken  by  connective  tissue,  and  the 
same  process  occurs  in  the  muscles. 

The  spinal  cord  when  examined  by  the  help  of  Nissl  and  Marchi 
stains  shows  some  involvement.  The  anterior-horn  cells  undergo  the 
same  degeneration  as  that  which  occurs  when  the  nerve  is  cut  across, 
and  slight  areas  of  degeneration  are  found  in  the  posterior  and  lateral 


'  "*;  \  ^^  :  -?i:5^ 


1         ..  H 


Fig.  39. — Arsenical  neuritis  (parenchymatous)  spinal  nerve  root. 

columns.  The  changes  are  very  slight  compared  with  those  in  the  nerves, 
and  in  the  writer's  experience  are  secondary. 

It  will  be  seen,  therefore,  that  in  multiple  neuritis  there  may  be:  (1) 
simple  degeneration;  (2)  parenchymatous  inflammation  with  some 
evidences  of  interstitial  neuritis  (degenerative  neuritis);  (3)  decided 
interstitial  neuritis  with  degeneration  of  nerve-fibres.  The  differences 
depend  on  the  intensity  of  the  poison. 

Diagnosis. — Multiple  neuritis  must  be  diagnosticated  from  diffuse 
or  transverse  myelitis,  anterior  poliomyelitis,  locomotor  ataxia,  spinal 


88 


DISEASES    OF    THE    NERVOUS    SYSTEM 


meningitis,  and  hemorrhage,  and  from  Landry's  paralysis.  Practically, 
dijffuse  myelitis  is  the  disorder  from  which  it  has  oftenest  to  be  distin- 
guished. From  this  it  is  recognized,  first,  by  investigating  the  cause  and 
onset.  Neuritis  begins  more  slowly  and  with  sensory  prodromata;  it 
affects  the  legs  and  feet,  especially  the  extensors,  and  if  it  ascends  it 
skips  the  hips  and  trunk  and  attacks  the  forearms.  There  is  more 
muscular  atrophy  than  in  myelitis;  the  knee-jerks  are  absent.  It  pro- 
gresses more  slowly,  and  after  four  or  eight  weeks  gradually  regresses. 


Fig.  40. — Interstitial  neuritis,  cross-section  of  3d  cranial  nerve. 

Electrical  degeneration  reactions  are  more  varied  and  decided.  There  is 
tenderness  over  the  muscles  and  nerves  and  peculiar  burning,  darting 
pains.  The  cutaneous  anaesthesia,  if  present,  is  not  so  extensive  and 
complete,  as  a  rule,  while  muscular  anaesthesia  is  more  decidedly  marked. 
There  is  very  rarely  involvement  of  the  sphincters  nor  are  there  bed- 
sores. There  may  be  belt-like  constrictions  felt  round  the  extremities, 
but  not  around  the  waist.  The  gradual  improvement  of  the  paralysis 
and  atrophy  and  eventual  recovery  confirm  the  diagnosis  of  neuritis. 


DISEASES    OF    THE    PERIPHERAL    NERVES  89 

The  presence  of  neuritis  of  the  cranial  nerves  would  strengthen  the  theory 
of  a  general  neuritis. 

From  poliomyelitis  it  is  distinguished  by  the  presence  of  pain  and  other 
sensory  symptoms,  the  early  fall  in  galvanic  irritability,  the  age  of  the 
patient  and  the  etiology. 

From  locomotor  ataxia  neuritis  is  distinguished  by  its  more  rapid 
onset,  the  presence  of  paralysis  and  atrophy  of  muscles,  paresis,  with 
degeneration  reactions,  and  the  absence  of  involvement  of  the  organic 
centres  and  pupils. 

Spinal  hemorrhage  usually  leads  soon  to  a  secondary  diffuse  mj^elitis 
easily  distinguishable  from  neuritis  by  the  characters  above  given.  Here 
there  is  also  usually  pain  in  the  back.  Spinal  meningitis  is  associated 
with  characteristic  pain,  tenderness  and  stiffness  along  the  back.  Acute 
ascending  paralysis  in  its  typical  form  shows  but  very  slight  sensory 
disorders,  and  no  wasting  or  change  in  electrical  irritability. 

The  complication  of  multiple  neuritis  and  myelitis  or  posterior 
sclerosis  is  possible,  but  is  very  rare.  In  the  former  case  the  ordinary 
symptoms  of  myelitis  are  added  to  those  of  neuritis.  In  locomotor 
ataxia  there  is  often  some  nerve  degeneration  and  occasionally  neuritis. 
The  nerve  degeneration  probably  causes  only  slow  atrophic  changes  and 
paresis;  the  neuritis  causes  pains,  anaesthesia,  skin  eruptions  and  local 
trophic  disorders. 

Prognosis. — Alcoholic  multiple  neuritis  is  a  serious  disease,  because 
of  its  associated  conditions.  Nearly  one-half  of  my  hospital  patients 
have  died,  mainly  because  they  continued  the  use  of  alcohol  after  paraly- 
sis appeared.  They  do  not  die  of  neuritis,  but  of  alcoholism,  pneumonia 
or  of  phthisis.  Other  forms  of  neuritis  rarely  cause  death.  The  great 
majority  recover  almost  completely.  It  may  be  from  six  months  to  two 
years  before  all  symptoms  disappear.     The  average  time  is  about  a  year. 

Treatment. — The  patient  needs,  first  of  all,  rest  in  bed.  The  limbs 
are  often  extremely  tender  and  the  patient's  pains  excruciating.  To 
relieve  these  the  legs  may  be  painted  with  menthol  and  enveloped  in 
cotton  batting.  In  other  cases  flannels  wrung  out  in  hot  water  and 
renewed  every  two  hours  give  relief.  Internally  phenacetin,  antipyrin 
or  other  coal-tar  products  may  be  given  for  the  pains.  Fluid  extract  of 
ergot  in  doses  of  5i-  to  §ii.  repeated  in  three  hours  sometimes  relieves 
pain.  In  the  early  stages,  salicylate  of  soda  in  doses  of  gr.  xx.  every  two 
or  three  hours  is  recommended.  If  there  is  a  great  deal  of  depression 
from  alcoholic  poisoning,  strychnine,  gr.  3^^o  Q-  3  h.,  and  aromatic  spirits 
of  ammonia,  §ss.  q.  3  h.,  should  be  used. 

There  is  no  drug  which  really  cuts  short  the  process.  The  best 
measures  for  this  purpose  are  rest,  thorough  cleansing  of  the  alimentary 
tract,  abstinence  from  alcohol  and  a  nourishing  diet. 


90  DISEASES    OF    THE    NERVOUS    SYSTEM 

After  the  acute  stage  is  passed  the  labile  galvanic  current  occasionally 
interrupted  fmay  be  applied,  5  to  10  ma.  for  ten  minutes  three  times 
daily.  Later,  by  the  sixth  week,  the  faradic  current,  massage  and  careful 
exercise  can  be  given.  At  this  time  or  earlier  (third  week),  strychnine, 
iodide  of  potassium,  arsenic  in  small  doses  and  tonics  may  be  given.  In 
old  cases  in  which  a  great  deal  of  paralysis  and  contracture  have  occurred, 
forcible  extension  of  the  limbs,  the  use  of  splints  and  rubber  muscles  are 
needed.  With  patience  and  perseverance  the  worst  chronic  cases  can 
eventually  be  brought  to  a  complete  recovery. 

Complicating  Forms  of  Neuritis  and  Neuritic  Degeneration. — Neuritis 
and  neuritic  degeneration  complicate  many  diseases,  but  they  especially 
mark  and  modify  subacute  and  chronic  rheumatism,  locomotor  ataxia, 
diabetes,  paralysis  agitans,  wasting  diseases  and  old  age. 

A  neuritic  degeneration  almost  always  affects  the  nerves  in  the  neigh- 
borhood of  an  old  rheumatic  joint.  The  chief  result  of  this  is  to  produce 
wasting  and  some  paresis  of  the  muscles  moving  the  joint  (Pitres  and 
Vaillard).  The  process  is  a  reflex  atrophy  (see  Arthritic  Muscular 
Atrophy) . 

In  locomotor  ataxia  parenchymatous  nerve  degeneration  is  very  often 
present.  It  does  not  produce  the  cardinal  symptoms  of  this  disease.  It 
does,  however,  cause  some  of  the  anaesthesia,  parsesthesia,  muscular 
atrophy,  sldn  dystrophies  and  visceral  crises. 

In  diabetes  the  neuritis  takes  the  form  of  the  sensory  type  of  multiple 
neuritis,  and  causes  parsesthesias  and  neuralgias  somewhat  hke  those  of 
locomotor  ataxia.  The  patient  has  sciatiC;  intercostal  and  other  neuralgic 
pains,  burning  or  numb  feet,  and  sometimes  loss  of  tendon  reflex.  The 
upper  extremities  are  rarely  affected. 

In  Wasting  Diseases  and  Old  Age. — In  various  wasting  diseases,  such 
as  phthisis,  cancerous  cachexia,  long-continued  fevers,  marasmus,  and 
in  senility,  a  simple  parenchymatous  degeneration  of  nerves,  with 
atrophy,  occurs  (Arthaud,  Koster,  Jappa).  The  symptoms  caused  by 
these  changes  are  very  shght.  They  contribute  to  the  weakness  and  wast- 
ing. In  old  age,  the  atrophy  of  the  nerves  is  one  cause  of  the  lessened 
sensibiHty  and  activity  of  the  skin  and  its  underlying  muscles. 

TUMORS  OF  NERVE 
Classification  and  Pathology-^Nerve  tumors  occur  as : 

1.  Nerve  hyperplasia. 

2.  True  neuromata. 

3.  Fibro-neuromata. 

4.  False  neuromata. 

1.  Hyperplasia  or  hypertrophy  of  nerve  trunks  is  very  rare.     Gen- 


DISEASES    OF    THE    PERIPHERAL    NERVES  91 

erally  the  increase  in  size  is  due  to  increase  of  the  interstitial  connective 
tissue.  Sometimes,  however,  there  is  an  increase  in  the  number  of  fibres 
and  thickening  of  the  myelin  sheath. 

2.  True  neuromata  are  also  very  rare,  and  occur  almost  exclusively 
on  spinal  nerves.  In  some  there  is  an  increase  in  medullary  fibres; 
in  others  only  an  increase  of  non-medullated  fibres,  i.e.,  only  the  axis- 
cylinders  and  neurilemma  increase.  They  occur  either  singly  or 
multiply. 

True  neuromata  are  usually  small,  ranging  from  1  cm.  (two-fifths 
of  an  inch)  to  6  cm.  in  diameter.  They  may  be  much  smaller  or  larger. 
They  are  usually  few  in  number,  but  may  be  very  numerous.  Gowers 
estimates  in  one  case  that  as  many  as  1000  were  present.  Even 
larger  numbers  have  been  observed.  They  rarely  cause  serious  symp- 
toms, but  may  produce  local  pains  and  paraesthesias. 

3.  Multiple  fibro-neuromata,  when  numerous,  constitute  a  condition 
known  as  neurofibromatosis  (Recklinghausen's  disease). 

This  is  a  rare  condition,  but  one  of  importance  because  sometimes 
these  tumors  develop  on  cranial  nerves,  gradually  increase  in  size  and 
become  practically  brain  tumors.  The  following  description  is  from  an 
article  upon  this  subject  by  Fraenkel  and  Hunt. 

The  tumors  occur  in  varying  size  from  that  of  a  pin's  head  to  that  of 
a  goose  egg.  In  some  cases  the  manifestation  of  the  disease  is  expressed 
by  a  solitary  growth  upon  one  nerve,  and  in  other  cases  several  hundred 
growths  have  been  present.  They  occur  on  all  cerebrospinal  and 
sympathetic  nerves  except  on  the  optic  and  the  olfactory.  The  acoustic 
nerve  has  been  shown  to  be  particularly  liable  to  the  formation  of  fibro- 
mata and  fibrosarcomata.  The  origin  of  these  tumors  is  usually  from 
the  endoneurium,  rarely  from  the  perineurium  and  exceptionally  from 
the  epineurium.  They  are  situated  either  centrally  within  the  nerve  or 
eccentrically  on  the  periphery  of  the  nerve.  The  general  conformation 
of  the  tumors  is  spherical  or  elliptical  and  in  generalized  cases  the  nodular 
outgrowths  give  the  nerve  a  convoluted  appearance,  sometimes  resem- 
bling a  rosary. 

Histologically,  the  fibroma  nervorum  is  made  up  of  connective-tissue 
elements,  which  present  all  the  variations  in  structure  between  the 
fibroma  molle  and  the  fibroma  durum. 

The  neurofibromata  are  usually  slowly  growing  tumors  of  a  benign 
nature.  Sometimes,  however,  they  undergo  a  retrograde  metamor- 
phosis and  show  cystic,  fatty  or  myxomatous  degeneration  or  they 
undergo  sarcomatous  transformation,  assuming  a  malignant  character. 

Neurofibromatosis  depends  often  on  a  hereditary  or  congenital  dis- 
position. It  is  frequently  associated  with  more  or  less  mental  impair- 
ment, imbecility,  and  somatic  stigmata  of  degeneracy.     Scrofulosis  and 


92 


DISEASES    OF    THE    NERVOUS    SYSTEM 


tuberculosis  are  often  found  in  the  histories  of  the  cases.     The  tumors  are 
not  painful  and  cause  no  symptoms  when  confined  to  the  skin. 


Fig.  41. — Neurofibromatosis.     (Fraenkel  and  Hunt.) 

Neurofibromatosis  may  show  itself  in  one  of  the  following    ways: 
(1)  Tubercula  dolorosa  (painful  tubercles,  Wood);  (2)  multiple  neuro- 


DISEASES    OF    THE    PERIPHERAL    NERVES  93 

fibromata  of  the  skin  (molluscum  fibrosum,  Recklinghausen's  disease); 
(3)  neuromata  or  neurofibromata  of  a  single  peripheral  nerve;  (4)  neu- 
roma plexiforme,  pachydermatocele,  and  elephantiasis  neuromatodes; 
(5)  generalized  neurofibromatosis;  neurofibromata  of  the  skin,  cerebro- 
spinal and  sympathetic  nerves. 

3.  Neurofibromata  of  individual  peripheral  spinal  nerves  (isolated 
neuromata)  are  surgically  well  known.  They  express  themselves  clin- 
ically by  parsesthesias  and  progressive  motor  weakness  of  the  peripheral 
nerve  type,  and  are  of  good  prognosis  when  recognized.  They  occur 
most  frequently  on  the  median  and  sciatic  nerves;  they  are  rarely 
without  symptoms  and  are  prone  to  give  rise  to  considerable  hyperses- 
thesias  and  little  paralysis. 

4.  False  Neuromata. — ^This  term  is  applied  to  the  various  nerve 
tumors  in  which  a  fibroma,  myxoma,  glioma,  sarcoma,  carcinoma  or 
syphiloma  grows  upon  or  in  the  nerve.  The  fibroneuroma  as  above  de- 
scribed is  really  a  false  neuroma  and  is  the  common  form;  glioneuroma 
has  been  observed  on  the  auditory  nerve.  Syphiloma  occurs  only  on  the 
intracranial  or  intraspinal  nerves.  Carcinoma  of  nerves  may  be  primary, 
but  is  generally  secondary,  and  is  of  scirrhous  or  medullary  type,  rarely 
the  colloid.  Leprous  neuritis  sometimes  forms  neurofibromatous  swell- 
ings. A  few  cases  have  been  observed  of  multiple  malignant  neuromata. 
Trauma  and  hereditary  influence  are  the  etiological  factors.  The  great 
nerve  trunks  are  oftenest  affected,  the  median,  sciatic  and  crural  ranking 
first.  The  tumors  start  from  the  perineurium;  they  are  at  first  spindle- 
shaped,  and  maj^  grow  very  large.  Sarcomatous  cells  are  oftenest  found 
in  them;  but  they  may  be  myxomatous,  fibromatous  or  mixed. 

Etiology. — Three  general  causes  exist  for  the  production  of  neu- 
romata, viz. :  1.  A  hereditary  or  a  neuropathic  predisposition,  which  tends 
to  cause  the  true,  the  multiple,  and  the  plexiform  neuromata.  2.  In- 
juries, surgical  operations;  these  cause  especially  the  fibroneuromata  of 
which  the  amputation  neuroma  is  an  example.  3.  Diathetic,  e.g.,  tuber- 
culous influences,  and  whatever  produces  the  various  tumor  formations, 
sarcoma,  carcinoma,  form  the  third  etiological  factor.  Neuromata  of 
the  plexiform  type  are  often  congenital.  Alultiple  neuromata  may  de- 
velop early  in  life.  Men  are  far  more  subject  to  multiple  neuromata 
than  women. 

Symptoms. — Neuromata  often  cause  no  symptoms.  Perhaps  the 
most  frequent  evidence  of  their  presence,  however,  is  pain  and  some 
tenderness.  The  pain  is  exacerbating,  and  may  be  stopped  sometimes 
by  pressure  on  the  nerve  above  the  tumor.  Parsesthesia,  anaesthesia, 
paralysis,  and  reflex  spasm  may  be  present.  Some  forms  of  intract- 
able headache  are  possibly  due  to  multiple  neuromata.  A  neuroma  upon 
one  of  the  cranial  nerves,  usually  the  acoustic,  may  develop  into  and  cause 


94 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


the  symptoms  of  a  brain  tmnor.  Hence  the  presence  of  nem^ofibromata 
of  the  skin  with  brain  symptoms  should  always  suggest  the  possible 
presence  of  an  intracranial  growth.  Multiple  and  plexiform  neuromata 
cause  symptoms  less  often  than  a  single  larger  neuroma.  A  neuroma  on 
the  pneumogastric  or  other  splanchnic  nerve  may  cause  severe  symptoms. 


Fig.  42. — Neuro-fibroma,  Recklinghausen's  disease. 

Multiple  (true)  neuromata  may  last  for  years  and  cause  no  serious  in- 
convenience. Malignant  neuromata  cause  always  such  symptoms  as 
would  naturally  follow  irritation  and  compression  of  a  nerve. 

The  treatment  of  neurofibromata  and  of  nerve  tumors  generally  is  usu- 
ally purely  surgical  when  any  treatment  is  indicated. 


CHAPTER  VIII 

MOTOR  DISORDERS  OF  CRANIAL  NERVES 

The  general  distribution  of  the  paralyses  from  injury  or  disease  of  the 
different  motor  nerves  is  shown  in  the  accompanying  table  of  cases.  I 
am  indebted  to  my  friends  Dr.  Wm.  P.  Wilkin  and  Dr.  Alexander  S. 
Leverty,  for  the  larger  part  of  the  work  of  compilation: 

Cranial-nerve  paralyses  (including  19  occurring  in  locomotor  ataxia.    .   206 

Spinal-nerve  paralyses 377 

Multiple  neuritis 114 

697 

The  cranial  nerves  having  motor  function  are  paralyzed  in  about  the 
following   frequency  : 

Facial,  136;  Oculo-motor,  52;  V,  X,  XI,  3. 

Taking  all  motor  nerves,  cranial  and  spinal,  one  finds  that  the  brachial 
plexus  and  its  branches  are  oftenest  affected  by  paralysis,  next  the  seventh 
cranial  nerve,  then  the  ocular  nerves,  and  last  the  lumbar  and  sacral  plexus. 
This  represents  the  frequency  in  a  neurologist's  experience.  In  general 
practice  and  especially  in  surgical  practice  there  would  be  fewer  cases  of 
cranial-nerve  disease  and  more  of  lumbar  and  sacral  palsies. 

THE  OCULAR  MUSCLES 

Anatomy. — The  motor  nerves  of  the  eye  are: 

(a)  The  third  or  oculo-motorius,  supplj^ing  the  internal,  superior  and  inferior 
recti,  inferior  obliquus,  the  levator  palpebrse,  the  ciliarjr  muscle,  and  constrictor  of 
the  iris. 

(6)  The  fourth  or  trochlearis  supplying  the  superior  oblique. 

(c)  The  sixth  or  abducens,  supplying  the  external  rectus. 

(d)  The  sympathetic,  consisting  of  fibres  from  the  cervical  cord  to  the  dilators  of 
the  iris,  to  its  blood-vessels,  and  to  the  unstriped  portion  of  the  levator  palpebrse  and 
to  the  unstriped  musculus  orbicularis. 

The  third  and  fourth  nerves  arise  from  a  series  of  nuclei  in  the  floor  of  the  aqueduct 
of  Sylvius.  They  leave  the  brain  at  the  anterior  edge  of  the  pons.  They  run  in  the 
cavernous  sinus  and  enter  the  orbit  through  the  sphenoidal  fissure. 

The  sixth  nerve  arises  from  a  nucleus  in  the  floor  of  the  fourth  ventricle.  It 
emerges  at  the  posterior  edge  of  the  pons,  runs  in  the  cavernous  sinus,  and  enters  the 
orbit  through  the  anterior  lacerated  foramen. 

The  nuclear  gray  matter  from  which  these  nerves  arise  is  made  up  of  a  series  of 
nests  of  cells  and  each  pair  supplies  a  different  set  of  muscles  of  the  ej^e,  as  shown  in 
the  diagrams  (Figs.  44  and  47). 

95 


96 


DISEASES    OF    THE    NERVOUS    SYSTEM 


The  nucleus  of  the  sixth  lies  farther  back  in  the  floor  of  the  medulla,  but  it  belongs 
to  the  same  serial  deposit  of  gray  matter  and  represents  the  continuation  of  the  ante- 
rior horn  of  the  spinal  cord  (Fig.  48). 

The  motor  nerves  of  the  eye,  third,  fourth  and  sixth,  are  closely  connected  with 
each  other  and  other  nerves  by  a  long  commissure,  the  posterior  longitudinal  bundle. 

The  fibres  of  the  third  and  sixth  nerves  pass  to  their  nuclei  on  the  same  side,  then 
decussate  and  pass  up  in  the  inner  part  of  the  crusta  to  the  frontal  part  of  the  prse- 
central  convolutions  of  the  cortex.  A  few  fibres  decussate  and  enter  the  nuclei  of 
the  opposite  side.     They  are  connected  with  the  internal  rectus  nucleus. 


Optic  cWasma 


Infundibulum 


Olfactory  bulb 


Left  corpus  mamiUare 


Substantia  perforata 
posterior 


Pedunculus  cerebri 


Olfactory  tract 


Optic  nerve 


Abdiicens  nerve 


Hypoglossal  nerve 


Substantia  perforata 
anterior 

Optic  tract 


Tuber  cinereum 
Oculomotor  nerve 

Trochlear  nerve 
Trigeminal  nerve 

Facial  nerve 
■Acoustic  nerve 
Nervus  intermedius 
'Glosso-pharyngeal  nerve 


Vagus  nerve 
Accessory  nerve 
Hypoglossal  nerve 

Fig.  43. — Showing  the  origin  of  the  nerves  at  the  base  of  the  brain. 


Medulla  Oblongata 

Medulla  spinalis  (cut) 


The  fibres  of  the  fourth  nerve  almost  entirely  decussate,  running  forward  a  long 
distance  before  they  finally  reach  their  nuclei.  Thus  it  appears  that  the  fourth  is 
the  only  cranial  nerve  except  the  optic  which  largely  decussates  before  reaching  its 
nucleus.  However,  those  fibres  of  the  third  which  supply  the  internal  rectus  also 
decussate,  as  already  stated. 

The  arrangement  and  composition  of  the  nuclei  of  the  oculo-motor  nerves  as  given 
by  Bing  is  as  follows : 

1.  A  small-celled  lateral  nucleus,  the  nucleus  of  Edinger  and  Westphal. 

2.  A  large-celled  lateral  nucleus. 

3.  A  small-celled  mesial  nucleus. 


MOTOR  DISORDERS  OF  CRANIAL  NERVES  97 

Of  these  the  longest  is  the  large-celled  lateral  nucleus.  It  contains,  ranged  one 
behind  the  other 

(a)  The  centre  for  the  levator  palpebra?  superioris. 
(6)  The  centre  for  the  rectus  superior. 

(c)  The  centre  for  the  rectus  internus. 

(d)  The  centre  for  the  obliquus  inferior. 

(e)  The  centre  for  the  rectus  inferior.     (See  Fig.  44.) 

The  fibres  from  (a)  and  (6)  arise  e:vclusively  from  the  nucleus  of  the  same  side, 
those  from  (e)  exclusively  from  that  of  the  opposite  side,  while  those  from  (c)  and  (d) 
arise  from  the  nuclei  of  both  sides. 

The  mesial  nucleus  is  the  centre  for  accommodation.  The  Westphal-Edinger 
nucleus  innervates  the  sphincter  pupilloe. 

The  mesial  and  lateral  small-cell  nuclei  send  fibres  which  pass  first  to  a  ganglion 
before  going  to  the  muscles  they  supply  and  they  belong  to  the  mid-brain  autonomic 
system . 

In  order  to  understand  the  peculiarities  of  eye  palsies,  to  be  de- 
scribed later,  the  relations  of  the  sixth  to  that  nucleus  of  the  third  nerve 
which  innervates  the  internal  rectus  must  be  understood.  In  turning 
the  eyes  to  one  side,  these  two  nuclei  and  their  nerves  act  together, 
causing  the  external  rectus  of  one  eye  and  the  internal  rectus  of  the 
other  to  contract  at  the  same  time.  The  impulse  from  the  brain  which 
does  this  decussates  and  acts  first  upon  the  sixth,  and  through  this  upon 
the  external-rectus  nucleus  of  the  same  side.  The  impulse  from  this 
nucleus  then  goes  to  the  third-nerve  fibres  of  the  same  side  and  thence 
to  the  internal  rectus.  This  can  be  better  understood  by  the  diagram, 
Fig.  45. 

Thus  lesions  in  the  brain  at  (a)  cause  paralysis  of  the  sixth  nerve 
of  the  opposite  side  and  internal  rectus  of  the  same  side.  The  eyes  turn 
toward  the  side  of  the  lesion. 

Lesions  in  the  pons  at  (5)  cause  paralysis  of  the  sixth  on  the  same 
side  and  internal-rectus  nucleus  of  the  opposite  side.  The  eyes  turn 
away  from  the  side  of  the  lesion. 

The  movements  of  the  eyeball  are  made  by  the  simultaneous  action  of 
several  muscles.  Most  of  them  act  as  their  names  indicate.  But  the 
obHque  muscles  help  to  depress  or  elevate,  and  then  help  to  rotate  in  or 
out  according  as  the  internal  or  external  rectus  is  acting. 

The  cortical  centres  for  the  eye  muscles  are  not  positively  known. 
Lesions  in  the  inferior  parietal  lobule  sometimes  cause  disorder  of  the 
third  nerve,  but  the  dominant  centres  are  in  the  prefrontal  lobe  at  the 
base  of  the  upper  and  middle  frontal  convolutions. 

As  the  optic  nerve  is  the  special  sensory  nerve  of  the  eye,  so  the  third, 
fourth,  sixth  and  part  of  the  seventh  nerves  are  the  motor  nerves.  By 
means  of  the  optic  nerve  and  its  receptive  and  refractive  apparatus,  the 
form,  color,  movement  and,  to  some  extent,  relations  and  distance  of 
objects  are  determined.     The  motor  nerves  adjust  the  eye  to  near  and 


98 


DISEASES    OF   THE    NEKVOUS   SYSTEM 


distant  objects,  inform  us  as  to  size  and  distance,  and  enable  us  to  follow 
moving  objects  and  to  shift  the  gaze  readily.  They  also  assist  in  protect- 
ing the  eye  against   injury. 

General  Symptoms. — It  is  impossible  always  to  disassociate  diseases 
of  the  oculo-motor  nerves  from  those  involving  their  nuclei.  Hence  we 
must  study  here  really  the  affections  of  the  whole  neurons.     These  are: 

(1)  Paralyses  or  ophthalmoplegias,  which  may  be  acute,  chronic, 
or  progressive;  (2)  pareses  or  myasthenic  states,  called  ordinarily  muscu- 


FiG.  44. — The  nuclei  of  the  motor  nerves  of  the  eye.     (Bing.) 

lar  asthenopias;  (3)  spasms,  such  as  strabismus,  nystagmus,  and  ble- 
pharospasm; (4)  reflex  disorders. 

There  are  many  special  terms  which  are  used  to  indicate  the  peculiar 
effects  of  various  paralyses  and  spasms  of  the  ocular  muscles  and  nerves, 
and  some  of  these  I  will  define  here: 

Erroneous  protection  is  a  condition  in  which  the  patient  is  unable 
to  judge  exactly  of  the  relation  of  external  objects  to  the  body;  for  this 
relation  is  determined  by  the  movements  of  the  ocular  muscles,  and,  these 
being  weak,  wrong  sensations  are  conveyed  to  the  brain.  Vertigo  may 
result  from  this  disturbance  of  muscular  sensation. 


MOTOR  DISORDERS  OF  CRANIAL  NERVES 


99 


Diplopia  or  double  vision  is  a  condition  clue  to  the  erroneous  sen- 
sation resulting  from  eye-muscle  palsy,  and  to  the  fact  that  the  images 
of  the  object  fall  upon  non-corresponding  retinal  fields.  Diplopia  is  simple 
or  homonymous  when  the  false  image  is  seen  on  the  same  side  as  the 
affected  eye.  When  a  red  glass  is  placed  over  this  eye  two  images  are 
seen,  the  red  one  being  on  the  side  of  the  eye  involved.  Diplopia  is 
heteronymous  or  crossed  when  the  false  image  is  on  the  side  opposite  to 
the  sound  eye. 

Conjugate  deviation  of  the  eyes  is  a  condition  in  which  both  ej^es 
turn  strongly  to  one  or  the  other  side.  It  may  be  paralytic  or  spas- 
modic. The  mechanism  is  a  complicated  one  and  not  perfectly  under- 
stood.    In  general,  destructive  lesions  of  the  brain  cause  a  paralytic 


Fig.  45. — Diagram  showing  the  probable  relations  of  the  nuclei  of  the  sixth  and 
of  the  internal  rectus  branch  of  the  third  to  the  brain.  P.  L.  B.,  Posterior  longitudinal 
bundle. 


deviation  toward  the  side  of  the  lesion,  and  irritative  or  compressing 
lesions  the  opposite  effect.  Destructive  lesions  in  the  pons  cause  a 
deviation  away  from  the  side  of  the  lesions.  The  palsy  then  involves 
the  sixth  cranial  nerve  and  the  branch  to  the  internal  rectus  from  the 
third.  The  sixth-nerve  nucleus  is  the  dominant  one,  and  impulses  from 
the  brain  go  to  it  first  (see  Fig.  45). 

In  diseases  of  the  motor  nerves  of  the  eye  it  is  found  that  the  paralyses 
occur  in  various  ways,  which  may  be  best  grouped  as  follows: 

Ophthalmoplegias 

1.  Paralyses  of  the  third  nerve.  \  Acute. 

2.  Paralyses  of  the  fourth  and  sixth  nerves.     /  Chronic. 

3.  Progressive  paralysis  of  all  or  part  of  these  nerves. 


100 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


THE  OPHTHALMOPLEGIAS 


I.  Paralysis   of   the    Oculo-motorius   or   Third   Nerve — Etiology. — 

The  commonest  causes  are  "exposure  to  cold"  (which  means  some  simple 
infection),  and  syphilis.  Other  causes  are  basal  meningitis,  intracranial 
tumors,  injuries,  compression  from  orbital  tumors,  the  diphtheritic 
poison;  excessive  use  of  tobacco  and  alcohol,  of  morphine,  or  other  drugs 
may  be  predisposing  causes.  Temporary  palsy  sometimes  occurs  in 
migraine  or  it  may  take  the  place  of  an  attack  of  migraine.  Partial 
or  temporary  palsies  also  occur  in  locomotor  ataxia,  in  diphtheria,  in 
certain  primary  muscular  atrophies  and  in  myasthenia  gravis. 

There  occurs,  in  rare  cases,  an  acute 
inflammatory  degeneration  of  the  nuclei 
of  the  ocular-muscle  nerves  similar  to 
acute  anterior  poliomyelitis.  This  con- 
dition has  been  called  ''polioencephalitis 
superior"  or  upper  bulbar  palsy. 

Symptoms. — When  all  the  muscles 
supplied  by  the  third  nerve  are  para- 
lyzed, there  is  dropping  of  the  lid  (ptosis, 
Fig.  46) ;  the  eye  can  be  moved  only  out- 
ward, and  downward  and  inward;  there 
is,  therefore,  divergent  strabismus  and 
double  vision  (diplopia).  The  pupil  is 
somewhat  dilated  and  does  not  contract 
to  light,  owing  to  paralysis  of  the  con- 
strictors of  the  iris;  and  there  is  loss  of 
power  of  accommodation,  so  that  the 
patient  cannot  read  print  close  to  him. 

The  patient  suffers  much  annoyance 
from  the  lid-drop  and  the  double  vision, 
and  there  are  sometimes  vertigo  and  pho- 
tophobia. Only  one  nerve  is  involved  at  a  time,  as  a  rule.  The  various 
eye  muscles  supphed  by  the  third  are  rarely  all  attacked.  The  levator 
may  escape  almost  entirely;  the  ciliary  muscle  and  iris  may  also  be  but 
slightly  involved;  while  these  latter  muscles  are  never  involved  alone 
in  ordinary  types  of  the  disease.  They  may  be  paralyzed  alone  in  diph- 
theria or  in  an  attack  of  migraine. 

The  affection  usually  runs  a  subacute  course,  lasting  but  a  few 
weeks.  Functional  palsies  last  but  a  few  days;  syphilitic  palsies  are 
usually  temporary  (one  to  three  weeks),  but  may  relapse  or  become 
extremely  obstinate.  Periodical  palsies  occur  every  year  or  six  months 
or  even  oftener;  they  last  a  few  days  or  weeks  and  are  accompanied  at 


Fig.  46. — Paralysis  of  3d  nerve 
with  ptosis.  {Wildbrandt  and 
Sanger.) 


MOTOR    DISORDERS    OF    CRANIAL    NERVES  101 

first  by  some  pain.     They  continue  to  recur  for  years.     They  may  be 
associated  with  attacks  of  migraine  and  are  migrainous  equivalents. 

In  diphtheritic  eye  palsies  the  first  three  or  four  nuclei  of  the  series 
making  up  the  origin  of  the  third  nerve  are  oftenest  affected,  causing 
paralysis  of  accommodation,  paralysis  of  the  iris  and  of  the  internal 
rectus,  the  three  muscles  concerned  in  accommodating  the  eye  to  near 
objects. 

Pathology. — In  the  rheumatic  palsies  there  is  a  low  grade  of  per- 
ipheral neuritis,  and  the  same  is  true  of  most  diphtheritic  and  other 
palsies  of  infectious  origin.  In  syphilitic  and  tabetic  palsies  there  is 
usually  a  specific  basilar  meningitis  involving  the  nerve-roots.  The 
meningitis  may  be  slight  or  may  amount  to  gummatous  deposit.  In 
functional  and  some  periodical  palsies  there  is  a  vasomotor  disturbance 
causing  congestion  or  anaemia  or  perhaps  simply  inhibition  of  the  nuclear 
centres.  Some  periodical  palsies  have  been  found  to  be  due  to  small 
tumors  involving  the  nerve-root.  In  rare  cases  there  is  primary  mus- 
cular atrophy  of  the  eyeball  nerves  or  primary  degeneration  of  the 
nuclear  centres.  The  nuclear  inflammation  forming  "polioencephalitis 
superior"  is  a  disease  probably  infectious  and  quite  similar  to  anterior 
poliomyelitis. 

Special  Symptoms. — One  must  determine  how  extensively  and  which 
of  the  muscles  supplied  by  the  third  nerve  are  involved. 

If  only  the  levator  palpebrse,  there  is  simply  falling  of  the  lid. 

If  the  external  eyeball  muscles  are  involved,  we  get: 

Limitation  of  movement  of  the  globe. 

Strabismus  and  secondary  deviation. 

Erroneous  projection. 

Double  vision  or  diplopia,  which  is  either  simple  or  crossed. 

If  the  motor  fibres  to  the  iris  are  paralyzed  there  is  immobility  and 
dilatation  of  the  pupil  and  there  is  a  loss  of  light  reflex.  If  the  light 
reflex  is  gone  but  accommodation  persists,  we  have  the  so-called  Argyll- 
Robertson  pupil. 

Iridoplegia  without  cycloplegia  is  most  significantly  present  in 
syphilitic  conditions.  Iridoplegia  may  also  occur  in  infections  like 
diphtheria  and  from  toxic  states  and  local  disease. 

If  the  motor  fibres  to  the  ciliary  muscle  are  paralyzed  we  have 
cycloplegia,  or  paralysis  of  accommodation.  It  also  may  occur  in  syphilis, 
tabes,  paresis  and  in  diphtheria.  It  sometimes  occurs  as  a  symptom 
in  migraine. 

Paralysis  of  Convergence. — The  internal  recti  muscles  may  be  quite 
normal  except  that  they  cannot  converge  the  eye.  When  this  is  the  case 
there  is  also  loss  of  the  associated  pupil  contraction.  This  form  of  paral- 
ysis sometimes  occurs.     It  is  inferred  that  there  are  two  separate  centres 


102  DISEASES    OF    THE    NERVOUS    SYSTEM 

for  contracting  the  pupil.  One  associated  with  the  Hght  reflex  and  one 
with  convergent  movement  (Turner). 

Paralysis  of  the  levator  palpehrcB,  causing  ptosis,  is  sometimes  seen 
alone.  A  functional  palsy  of  the  lids  sometimes  occurs  in  anaemic  and 
nervous  people  at  the  time  of  waking.  It  is  a  temporary  morning  or 
waking  ptosis.  Ptosis  is  a  frequent  and  early  symptom  of  myasthenia 
gravis. 

Paralysis  of  the  sympathetic  fibres  of  the  eye  causes  the  Horner 
syndrome,  viz.:  contraction  of  the  pupil  (myosis)  from  the  unopposed  ac- 
tion of  the  third  nerve.  There  is  also  a  slight  retraction  of  the  eyeball, 
a  narrowing  of  the  palpebral  fissure,  sweating  of  the  face  on  the  affected 
side  and  lessened  intraocular  tension.  The  pupil  does  not  dilate  when 
the  skin  of  the  cheek  or  neck  is  irritated,  a  condition  known  as  loss  of 
oculo-skin  reflex  and  it  does  not  dilate  in  the  dark  or  respond  to  an  in- 
stillation of  cocaine.  On  the  other  hand  the  pupil  contracts  to  near 
vision  and  convergence.  The  spinal  centre  is  in  the  first  dorsal  and 
eighth  cervical  segment.  The  fibres  pass  out  through  the  first  and  second 
anterior  dorsal  roots,  scend  in  the  cervical  sympathetic,  pass  to  the 
Gasserian  ganglion  and  thence  through  the  first  division  of  the  trigeminus 
to  the  pupil. 

II.  Paralysis  of  the  Fourth  Nerve. — This  is  a  rare  affection  and  not 
always  easily  detected.  The  causes  are  much  the  same  as  those  of  palsy 
of  the  third  nerve.  The  symptoms  are  slight  convergent  strabismus 
when  the  eye  is  moved  downward  and  diplopia  on  looking  down.  There 
is  defect  in  the  movements  of  the  eye  downward  and  outward. 

III.  Paralysis  of  the  sixth  nerve  (abducens)  is  the  most  frequent 
of  eye  palsies,  and  occurs  especially  often  in  syphilis  and  in  locomotor 
ataxia.     It  causes  convergent  strabismus  and  double  vision. 

Progressive  Ophthalmoplegia. — ^Besides  the  palsies  already  described, 
there  occur  certain  forms  which  have  a  peculiar  origin  and  course.  They 
begin  slowly,  as  a  rule,  and  steadily  progress.  In  some  cases  only  do 
they  reach  a  certain  stage  and  then  remain  chronic.  They  often  affect 
the  third,  fourth  and  sixth  nerves  together.  In  accordance  with  the 
muscles  invaded,  these  palsies  are  called  external,  internal,  partial  and 
total.  Thus  if  those  branches  of  the  third  nerve  supplying  the  iris  and 
ciliary  muscle  are  involved  alone,  it  is  ophthalmoplegia  interna;  if  the 
other  branches  are  involved,  it  is  called  ophthalmoplegia  externa. 

Definition. — Progressive  ophthalmoplegia  is  a  degenerative  disease 
of  the  nuclei  of  the  motor  nerves  of  the  eye.  It  is  in  most  cases  the  same 
disorder  as  of  bulbar  paralysis  and  progressive  muscular  atrophy. 

Etiology. — It  develops  between  the  ages  of  fifteen  and  forty,  but 
may  occur  later.  The  sexes  are  equally  affected.  Lead,  diphtheria, 
traumatism,  syphilis,  appear  sometimes  to  be  the  cause.     It  may  compli- 


MOTOR    DISORDEES    OF   CRANIAL  NERVES  103 

cate  locomotor  ataxia;  more  often  it  forms  part  of  progressive  muscular 
atrophy. 

The  sijm-ptoms  are  often  not  noticed  until  the  disease  is  well  advanced. 
The  vision  is  not  disordered,  and  there  is  only  a  gradual  limitation  of 
mobility  of  the  eyeball.  A  slight  drooping  of  the  lids,  causing  a  sleepy 
look,  or  a  slight  squint,  usually  divergent,  is  noticed.  Then  upon  ex- 
amination it  is  found  that  the  eyes  are  immovable  and  cannot  follow  the 
finger,  except  to  a  slight  extent.  The  peculiar  physiognomy  which  re- 
sults is  known  as  the  "Hutchinson  face."  The  iris  reacts  to  accommo- 
dation and  light  usually.  Double  vision  may  be  present.  Usually  the 
patient  accustoms  himself  to  monocular  vision.  The  disease  lasts  a  long 
time,  and  it  may  become  stationary.  If  complicated  with  progressive 
muscular  atrophy,  however,  the  course  is  relatively  rapid,  death  occur- 
ring from  the  latter  disease  in  two  or  three  years. 

Pathological  Anatomy. — In  all  progressive  cases  there  is  a  degenera- 
tive atrophy  of  the  nuclear  cells.  In  a  few  stationary  cases  the  anatom- 
ical change  is  that  of  neuritis. 

The  treatment  is  that  for  the  disease  which  it  complicates  or  the  con- 
dition which  causes  it.  That  is  to  say,  it  is  the  treatment  for  locomotor 
ataxia,  progressive  muscular  atrophy,  syphilis  or  lead  poisoning.  Iodide 
of  potassium,  strychnine,  arsenic,  and  phosphorus  may  be  given.  Elec- 
tricity is  of  no  value.  General  tonic  measures  and  rest  to  the  eyes  should 
be  employed. 

Muscular  Asthenopia  and  Muscular  Insufficiencies. — ^This  is  a  term 
employed  to  indicate  a  lack  of  equilibrium  of  the  muscles  of  the  eye,  as 
a  result  of  which  the  visual  axes  cannot  be  kept  parallel  without  an  effort. 
This  effort  is  often  unconscious,  and  shows  itself  only  by  a  ready  tiring 
of  the  eye  on  attempting  to  read  or  by  the  production  of  headaches  and 
cerebral  paresthesias.  Examination  of  the  eye  by  means  of  prisms  re- 
veals the  special  character  of  the  trouble.  The  term  is  usually  apphed 
to  functional,  congenital  and  neurasthenic  weaknesses,  not  to  those  due 
to  organic  disease  or  severe  toxaemias. 

When  the  eye  muscles  act  normally,  the  condition  is  called  one  of 
orthophoria.  When  some  of  the  muscles  are  weak  it  is  called  heterophoria. 
There  are  various  forms  of  heterophoria,  viz. :  esophoria,  a  tending  of  the 
visual  lines  inward,  from  weakness  of  the  externi;  exophoria,  a  tending  of 
visual  lines  outward ;  hyperphoria,  a  tending  of  the  visual  line  of  one  eye 
above  its  fellow. 

The  condition  is  tested  in  various  ways.  The  simplest  is  this:  Re- 
fractive errors  having  been  corrected,  a  series  of  prisms  is  placed  over  the 
eye,  at  first  with  the  base  inward,  while  the  patient  looks  at  a  candle 
20  feet  distant.  The  prisms  are  increased  in  strength  until  the  patient 
can  no  longer  coalesce  the  images.     The  degree  of  prism  is  noted,  and 


104  DISEASES    OF   THE    NERVOUS    SYSTEM 

this  indicates  the  strength  of  abduction  or  of  the  externi.  The  same 
process  is  gone  through  with  for  the  interni,  the  base  of  the  prism  being 
out.  The  externi  should  overcome  a  prism  of  about  8°,  the  interni  one 
of  23°  to  25°  or  more.  There  are  great  individual  variations,  and  there 
is  also  considerable  variation  in  individuals. 

For  details  of  the  technic  for  testing  heterophoria  the  reader  can 
best  consult  special  works. 

Muscular  asthenopia  is  said  to  cause  a  disturbance  of  vision,  vertigo 
migraine,  cerebral  parsesthesia,  and  pains  in  the  head,  more  particularly 
in  the  occipital  and  cervical  region.  It  may  be  a  factor  in  producing 
choreic  twitchings  in  the  face.  In  neurasthenic  persons  it  may  cause  a 
wider  range  of  nervous  symtpoms.  It  is  said  to  be  a  factor  in  causing 
epilepsy,  chorea,  and  hysteria.  The  author  cannot  accept  this  latter 
view,  and  believes  that  the  importance  of  muscular  asthenopia  in  causing 
general  nervous  symptoms  is  not  great.  Much  of  it,  if  not  all,  may  be 
relieved  after  correcting  refractive  errors  by  helping  the  general  health 
of  the  patient. 

The  treatment  of  it,  after  all  myopia,  or  hypermetropia,  or  astigma- 
tism, if  present,  is  relieved,  consists  in  building  up  the  general  health, 
in  the  systematic  use  of  prisms  for  training  the  muscles,  and  the  wearing 
of  proper  glasses.  Sometimes  graduated  or  complete  tenotomies  are 
advisable. 

SPASMODIC    DISEASES    OF    THE    OCULAR    MUSCLES 

These  are:  (1)  Conjugate  deviation  from  spasm;  (2)  irregular  and 
associated  spasms  from  convulsive  and  irritative  brain  disorder;  (3) 
nystagmus. 

Spasmodic  conjugate  deviation  occurs  from  an  irritating  lesion  of  the 
ocular  nuclei  or  of  the  brain  in  its  cortical  motor  and  mid-brain  tracts. 
Irregular  spasmodic  movements  occur  in  meningitis,  hydrocephalus, 
and  in  lesions  involving  the  semicircular  canals.  Peculiar  associated 
spasms  occur  in  hysterical  attacks.  Various  spasmodic  movements  and 
contractions  of  individual  eye  muscles  occur  from  ocular  disease,  errors  of 
refraction,  muscular  weakness,  and  paralysis  of  certain  eye  muscles. 

Rhythmical  spasm  or  nystagmus  occurs  as  the  result  of  hereditary 
visual  weaknesses,  of  refractive  errors  of  various  kinds,  in  albinoes,  and 
in  chronic  hydrocephalus.  It  is  found  usually  in  neurotic  persons  who 
have  ocular  defects,  in  multiple  sclerosis,  and  sometimes  in  chorea. 
It  occurs  also  in  hereditary  ataxia,  tumors,  especially  of  the  cerebellum, 
and  mid-brain,  and  in  meningitis.  It  occurs  in  miners  and  is  called 
miner's  nystagmus. 

In  nystagmus  the  oscillation  of  the  eyeballs  is  usually  lateral.  It 
may  be  brought  out  when  slight  in  degree  by  causing  the  patient  to  look 


MOTOR  DISORDERS  OF  CRANIAL  NERVES 


105 


steadily  to  one  side.  Vertical  and  a  kind  of  rotating  nystagmus  some- 
times occur,  and  are  due  to  lesions  of  the  mid-brain  and  its  vestibular 
connections. 

Spasm  of  the  levator  palpebr^  is  sometimes  seen  and  is  usually  tonic. 

The  above  troubles  are  all  symptomatic,  and  their  treatment  de- 
pends upon  correction  of  some  local  disease  or  serious  cerebral  lesion. 

THE  MOTOR  BRANCH  OF  THE  FIFTH  CRANIAL  NERVE 

The  anatomy  of  this  nerve  is  described  under  the  head  of  the  neu- 
ralgias of  the  trigeminus. 


Nuc.  iii  E.  W. 
Nuc.  iii  lat. 

Nuc.  iii  med. 
Nuc.  iv. 

Locus  coeruleiis 
Nuc.  Mot.  V. 


Nuc.  vi. 

Nuc.  Mot.  vii. 

Nuc.  sal.  sup. 

Nuc.  sal.  inf. 

Trigonum  vagi. 

Nuc.  dorsalis  x. 

Nuc.  ambiguus. 

Nuc.  xii. 


colliculus  superior, 
corpus  geniculatum  Med. 

collicus  inferior. 
N.iv. 

Pons. 

N.  V. 

Nuc.  sensor  v. 
Eminentia  teres. 

Nuc.  vestibularis. 
Nuc.  cochlearis. 
Nuc.'fasc.  solitarius. 

Nuc.  spinalis  v. 
Nuc.  com.  cajal. 


Fig.  47. — Showing  the  position  of  the  cranial  nerve  nuclei  in  the  pons-meduUa.     (Herrick.) 

The  diseases  of  the  motor  branch  of  the  trigeminus  are  rare,  and 
generally  symptomatic  of  some  more  general  disorder. 


106  DISEASES    OF    THE    NEEVOUS    SYSTEM 

Trismus  (lockjaw)  is  the  only  important  independent  affection  of  this 
motor  nerve.     It  is  a  tonic  spasm  of  the  muscles  of  mastication. 

Etiology. — It  occurs  in  infants,  usually  through  infection  from  the 
umbilicus.  It  is  then  known  as  trismus  nascentium.  It  forms  part  of 
the  symptoms  of  tetanus,  tetany  and  rabies.  It  may  be  symptomatic 
of  brain  disease,  and  forms  one  of  the  manifestations  of  the  epileptic  fit 
and  of  hysteria.  There  may  be  a  reflex  trismus  from  irritations  of  the 
teeth  and  jaw  and  from  gastro-intestinal  trouble.  It  may  be  associated 
with  a  trigeminal  neuralgia. 

Symptoms. — There  is,  as  shown  above,  a  symptomatic,  an  infec- 
tious, a  reflex,  and  a  hysterical  trismus.  In  all,  the  symptoms  are  very 
manifest.  The  jaws  are  firmly  locked  and  the  masseters  and  temporals 
stand  out.  If  the  disease  is  unilateral,  which  is  rarely  the  case,  the 
lower  jaw  is  pushed  over  toward  the  sound  side. 

The  treatment  of  both  tonic  and  clonic  spasms  depends  upon  the 
cause.  Symptomatically,  morphine  is  to  be  given,  and  later  the  anti- 
spasmodics, such  as  the  bromides  and  chloral.  In  rheumatic  cases, 
hot  applications  and  diaphoretics  are  indicated. 

THE  FACIAL  NERVE 

Anatomy. — The  facial  nerve  has  its  primary  origin  in  a  single  nucleus  deeply  sit- 
uated in  the  lower  part  of  the  pons  (Fig.  48).  It  belongs  to  the  same  series  of  nuclei 
as  the  vagus,  glossopharyngeal,  and  spinal  accessory;  in  other  words,  it, is  a  prolonga- 
tion of  the  lateral  horn  of  the  spinal  cord.  It  receives  some  fibres  from  the  hypoglossal 
nerve  which  supplies  the  orbicularis  oris,  in  part.  The  deep  facial  fibres  curve  down 
and  out  around  the  nucleus  of  the  sixth  nerve  (Fig.  48).  The  cortical  origin  of  the 
seventh  nerve  is  in  the  lower  part  of  the  prsecentral  convokition.  The  upper  branch 
of  the  facial  which  supplies  the  muscles  of  the  upper  part  of  the  face  has  a  cortical 
origin  from  each  hemisphere,  so  that  a  lesion  of  one  cerebral  hemisphere  does  not  cause 
its  paralysis.  The  fibres  from  the  cortex  pass  down  through  the  knee  of  the  internal 
capsule  and  enter  the  crusta  at  the  inner  side  of  the  pyramidal  tract.  They  decussate 
and  reach  the  nucleus. 

The  nerve  has  its  exit  at  the  posterior  edge  of  the  pons,  external  to  the  sixth  nerve. 
It  has  then  to  take  a  long  course  through  the  internal  auditory  meatus  and  Fallopian 
aqueduct.  During  its  course  here  it  receives  communications  from  the  nerve  of 
Wrisberg  and  from  the  great  superior  petrosal  nerve.  It  sends  a  motor  branch  to 
the  stapedius  muscle  in  the  middle  ear  and  it  gives  off  the  corda  tympani  nerve. 
The  nerve  passes  out  through  the  stylo-mastoid  foramen  and  supplies  all  the  muscles 
of  the  face,  the  stylo-hyoid,  posterior  belly  of  the  digastric,  the  buccinator  and  the 
platysma  myoid.  It  does  not  supply  the  soft  palate  or  the  muscles  of  mastication. 
The  facial  nerve  is  a  mixed  nerve  and  has  a  sensory  part.  The  fibres  of  this  sensory 
root  arise  in  the  geniculate  ganglion.  They  pass  centrally  into  the  medulla  to  a 
small  nucleus  near  that  of  the  glossopharyngeal;  the  peripheral  fibres  pass  in  the 
nerve  of  Wrisberg  and  communicate  with  the  motor  portion  of  the  seventh. 

Motor  Function. — As  already  stated,  the  facial  nerve  is  a  motor  nerve  for  the 
muscles  of  the  ear  and  face  and  for  the  stapedius  muscle,  a  muscle  which  antagonizes 
the  tensor  tympani. 


MOTOR  DISORDERS  OF  CRANIAL  NERVES 


107 


Sensory  Function. — The  nerve  of  Wrisberg  and  its  ganglion  contains  a  few  vestigial 
fibres  which  supply  cutaneous  sensation  to  a  small  area  in  the  concha  and  to  the 
posterior  wall  of  the  external  meatus  (J.  Ramsay  Hunt). 

Special  Sense. — Fibres  of  the  special  sense  of  taste  originating  in  the  medulla 
pass  probably  in  the  second  and  third  branch  of  the  trigeminal  nerve,  thence  to 
Meckel's  ganglion,  then  through  the  large  superior  petrosal  nerve  to  the  geniculate 
ganglion,  on  through  it  and  thence  in  the  trunk  of  the  facial  to  a  point  near  its  exit 
from  the  skull;  there  they  leave  in  the  chorda  tympani  nerve  to  join  with  the  lingual 
branch  of  the  fifth  nerve  and  supjaly  the  sense  of  taste  to  the  anterior  two-thirds 
of  the  tongue  (Fig.  49).  It  seems  probable  that  in  some  cases  the  fibres  for  the 
sense  of  taste  come  from  the  glossopharyngeal  through  the  nerve  of  Wrisberg  and 
thus  pass  into  the  chorda  tympani. 

Secretory. — Fibres  stimulating  the  secretion  of  saliva  run  in  the  nerve  of  Wrisberg, 
the  geniculate  ganglion  and  the  chorda  tympani  to  the  corresponding  side  of  the 
tongue,  and  when  this  nerve  is  irritated  or  paralyzed  there  are  disturbances  in  saliva- 
tory  secretion. 


Fig.  48. — ^Longitudinal  section  showing  position  of  the  nuclei  of  medulla.     (Edinger.) 

Fibres  which  stimulate  tear  secretion  pass  in  the  seventh  into  the  geniculate 
ganglion,  thence  through  the  great  superior  petrosal  nerve,  and  thence  to  the  lach- 
rj^mal  branch  of  the  trigeminus. 

The  connections  of  the  facial  nerve  with  other  nerves  in  its  course  through  the 
aqueduct  of  Fallopius  make  it  possible  to  determine  the  location  of  the  different 
lesions  which  affect  the  facial  nerve  in  this  part. 

The  facial  nerve  being  mainly  motor,  its  diseases  are  spasmodic  and  paralytic. 
The  two  common  types  are  facial  tic  and  facial  palsy,  but  there  are  other  minor 
forms. 

The  spasmodic  disorders  are:  (1)  diffuse  facial  spasm  or  mimic  tic  and  (2)  spasm 
of  single  branches,  including  (a)  blepharospasm  and  (b)  nictitating  spasm. 

Facial  Spasm  {Mimic  Tic). — :This  is  a  disease  characterized  by  inter- 
mittent, involuntary  twitchings  of  the  facial  muscles.  It  is  always 
chronic  and  generally  unilateral. 

Etiology. — It  is  a  disease  of  middle  and  later  life,  and  occurs  oftener 
in  women;  there  is  usually  a  neuropathic  constitution;  it  is  not  hereditary. 
The  exciting  causes  are  shock,  injury,  and  local  irritations.  It  often 
has  a  reflex    cause,   usually   from   irritation   of   some  branch  of  the 


108 


DISEASES    or    THE    NERVOUS    SYSTEM 


trigeminus.  It  is  sometimes  associated  with  tic  douloureux.  It  may 
have  an  origin  in  reflex  irritation  of  the  sensory  part  of  the  seventh 
nerve,  viz.,  the  geniculate  ganglion  and  nerve  of  Wrisberg.  Organic 
diseases,  such  as  tumors  and  softening,  affecting  the  nerve  nucleus  in 
the  pons  or  the  cerebral  centres,  cause  a  symptomatic  tic,  but  not  the 
true  disease.  Thus  we  may  have  a  post-hemiplegic  tic  or  a  tic  due  to 
cortical  lesion  and  associated  with  epilepsy.  A  facial  tic  may  also  be 
caused  by  irritation  or  disease  of  the  nerve  trunk  or  of  its  nucleus. 
It  sometimes,  though  rarely,  follows  a  facial  palsy. 

Symptoms.^ — The  disease  usually  begins  slowly  and  the  orbicularis 
muscle  and  zygomatici  are  earliest  affected.     It  rarely  goes  above  the 


<<e  Jatbbsoii. 
Umparai  nificrf. 


Fig.  49. — Showing  the  usual  course  of  the  taste  fibres  in  the  seventh  and 
fifth  nerves.     {Krause.) 

eyebrows,  i.e.,  to  the  corrugator  supercilii  and  frontalis.  The  lower 
branch  of  the  facial  is  little  affected.  The  spasm  is  at  first  a  clonic 
one;  the  muscles  of  the  face  are  affected  by  a  series  of  lightning-like 
twitches,  with  intervals  of  rest.  Sometimes,  however,  the  contraction 
becomes  tonic  and  lasts  several  seconds  or  more.  There  is  no  pain. 
The  spasm  is  increased  by  emotions,  nervous  excitement,  conversation, 
exposure  to  light  and  cold,  and  is  at  its  worst  when  the  patient  himself 
is  most  depressed.  It  is  a  very  good  gauge  of  the  general  nervous  stability 
of  the  patient.  There  is  no  paralysis  or  atrophy  and  there  are  no  se- 
cretory or  trophic  symptoms.  The  taste  fibres  are  rarely  involved, 
though  occasional  subjective  sensations  of  taste  have  been  felt.  The 
electrical  irritability  is  either  unchanged  or  slightly  increased. 


MOTOR  DISORDERS  OF  CRANIAL  NERVES  109 

Associated  movements  of  the  eyes,  of  the  jaw  muscles  and  cheek 
muscles  are  sometimes  seen.  Pressure  over  the  motor  points  of  the 
nerve  will  sometimes  arrest  the  movements  for  a  time.  The  disease  is 
a  unilateral  one.     It  lasts  for  years  and  even  for  the  lifetime. 

Pathology. — There  is  no  known  anatomical  change  in  idiopathic 
cases.  The  disease  is  allied  in  character  to  wry-neck  and  other  chronic 
tics.  In  these  cases  it  is  probably  the  expression  of  some  functional 
deterioration  of  the  higher  reflex  centres.  The  disease  is  sometimes 
a  pure  reflex  neurosis  from  ocular  or  dental  or  other  irritations.  In  the 
facial  tic  that  sometimes  follows  hemiplegia  (nuclear  tic)  there  is  probably 
some  degenerative  change  in  the  nucleus  of  the  facial. 

Diagnosis. — ^Idiopathic  facial  spasm  is  chronic,  unilateral,  unac- 
companied by  pain  or  paralysis.  It  is  distinguished  from  facial  spasms 
of  organic  origin  by  the  fact  that  the  latter  always  have  some  other 
symptoms.  Thus  facial  habit  chorea  is  bilateral;  spasm  from  cortical 
disease  is  attended  by  disturbance  of  consciousness  and  comes  on  in 
paroxysms;  the  spasm  occurring  after  hemiplegia  is  usually  tonic,  and 
so  is  hysterical  facial  spasm. 

Prognosis. — The  disease  is  in  most  cases  incurable,  especially  after 
it  has  lasted  some  time.  If  a  reflex  cause  exist,  the  prognosis  is  better. 
Life  is,  however,  never  endangered  by  it. 

Treatment. — The  most  important  thing  is  attention  to  the  general 
health,  removal  of  all  depressing  influences,  rest,  and  freedom  from 
excitement.  Among  specific  remedies  the  bromides,  parathyroid  ex- 
tract, the  phosphates,  gelsemium,  conium,  hyoscyamus,  codeine  and 
morphine  are  recommended.  Morphine  is  useful,  but  must  be  tried 
carefully  and  in  small  doses.  Conium  lessens  the  spasm,  but  this  drug 
has  to  be  given  in  large  doses  and  is  not  entirely  free  from  danger. 
Hyoscine  and  gelsemium  sometimes  do  good.  Careful  examination 
of  the  teeth,  eyes,  nose,  stomach  and  uterus  for  reflex  irritation  is 
imperative. 

Neurectomy  of  the  supra-orbital,  continuous  pressure  on  the  motor 
points,  stretching  the  nerve  itself  are  all  measures  which  may  be  con- 
sidered valueless.  Freezing  the  skin  over  the  nerve  with  chloride  of 
methyl  has  been  recommended  by  Mitchell.  Blistering  and  cauteriza- 
tion are  needless  inflictions.  The  ansesthetization  of  the  conjunctiva 
with  cocaine  is  often  helpful,  both  in  diagnosis  and  treatment.  Sys- 
tematic training  exercises,  in  which  the  patient  sits  before  a  mirror  and 
tries  to  hold  the  spasm  in  control,  and  systematic  facial  and  head  move- 
ments help  and  may  even  cure  these  cases.  I  have  seen  a  case  appar- 
ently relieved  by  extract  of  parathyroid  three  times  a  day.  Injections 
of  alcohol  into  the  nerve  have  cured  some  cases  (Patrick). 

Blepharospasm  is  the  name  given  to  a  spasm,  mainly  tonic,  of  the 


110  DISEASES    OF    THE    NERVOUS    SYSTEM 

orbicularis  palpebrarum.  It  is  generally  caused  by  diseases  of  the 
eye,  and  its  nature  and  treatment  are  matters  belonging  to  ophthal- 
mology.    It  is  a  rare  symptom  of  hysteria. 

Nictitating  or  winking  spasm  is  a  clonic  spasm  of  the  orbicularis, 
and  usually  forms  part  of  habit  chorea  or  is  a  symptom  of  hysteria. 

Tonic  facial  spasm  is  sometimes  seen  in  major  hysteria, 

FACIAL  PALSIES 

The  paralyses  of  the  facial  nerve  may  be  due  to  lesions  that  are 
cerebral  and  supra-nuclear,  or  nuclear  and  peripheral. 

Facial  palsy  of  supra-nuclear  origin  is  almost  invariably  an  accom- 
paniment of  hemiplegia  and  is  due  to  hemorrhage,  softening,  inflamma- 
tion, or  tumor  of  the  brain.  The  lower  two  branches  of  the  facial  are 
chiefly  involved. 

Facial  palsy  of  nuclear  origin  is  very  rare  and  is  an  accompaniment 
of  glosso-labial  palsy,  of  diphtheritic  palsy,  or  of  gross  lesions  of  the 
pons. 

Peripheral  facial  palsy  {BelVs  palsy)  is  the  common  type  of  facial 
paralysis,  making  up  over  80  per  cent,  of  cases.  It  is  of  infra-nuclear 
(peripheral)  or  nuclear  origin. 

Etiology. — The  typical  cases  of  this  disease  are  due  to  exposure  and 
so-called  "rheumatic  influences"  with  infection.  After  this  the  most 
frequent  causes  are  ear  disease,  trauma,  syphilis  and  tumors.  Males 
are  oftener  affected,  and  the  common  age  is  between  twenty  and  forty. 
It  is  more  frequent  in  the  winter  and  in  temperate  climates.  It  is  not 
hereditary,  but  it  may  be  congenital.  A  neuropathic  tendency  predis- 
poses to  it.  Meningeal  syphilis  sometimes  causes  an  isolated  facial 
palsy,  although  it  is  apt  to  leave  this  nerve  alone.  Facial  palsy  may 
occur  in  multiple  neuritis,  when  it  is  often  bilateral.  Non-typical  and 
accidental  cases  of  peripheral  facial  palsy  are  due  to  injuries,  fracture  of 
the  petrous  bone,  or  ear  disease.  Forceps  pressure  in  difficult  labor 
causes  some  cases.  The  ordinary  cases  are  mostly  due  to  microbic 
infections  similar  to  those  of  ''colds"  and  influenza. 

Symptoms. — The  disease  comes  on  rather  suddenly,  and  reaches 
its  height  within  a  few  hours  or,  at  most,  two  or  three  days.  Pre- 
ceding and  accompanying  the  onset  there  may  be  some  pain  about  the 
ears,  and  a  little  swelling  is  sometimes  seen. 

The  patient  feels  a  subjective  discomfort  on  the  paralyzed  side 
of  the  face.  He  finds  that  he  cannot  completely  shut  the  eye  and  if  he 
tries  to  chew  on  the  affected  side,  food  gets  between  the  teeth  and  cheek. 
He  cannot  pucker  the  lips,  and  his  speech  is  a  little  muffled.  The 
appearance  of  the  face  is  most  characteristic. 


MOTOK  DISORDERS  OF  CRANIAL  NERVES 


111 


On  the  affected  side  the  wrinkles  are  smoothed  out,  the  angle  of  the 
mouth  is  lower,  the  mouth  is  drawn  at  first  to  the  sound  side,  and  ow- 
ing to  this  distortion  the  tongue  appears  not  to  be  protruded  straight. 
The  base  of  the  tongue  is  lowered  through  paralysis  of  the  stylo-hyoid 
and  posterior  belly  of  the  digastric.  In  laughing  or  other  emotional 
movements  of  the  face,  the  trouble  is  most  clearly  brought  out.  But 
the  most  characterized  appearance  is  produced  by  telling  the  patient 
to  shut  the  eyes  tightly  and  draw  out  the  angles  of  the  mouth  so  as  to 
show  the  teeth  (Fig.  50).  The  eye  on  the  palsied  side  is  not  closed  and 
the  eyeball  turns  up,  showing  the  white  of  the  eye.     In  a  forced  attempt 


Fig.  50. — Patient  with  left  facial  palsj^  trying  to  close  both  eyes  and'show  the  teeth. 

at  closing  the  eye,  the  upper  lid  may  be  drawn  up.  In  children,  and  in  the 
young  and  plump,  the  differences  in  the  two  sides  of  the  face  when  at  rest 
are  not  marked,  especially  in  the  slighter  cases.  The  nostril  on  the  af- 
fected side  does  not  expand  on  forced  inspiration;  the  eye  is  apt  to  be 
watery  and  the  conjunctiva  somewhat  injected. 

After  a  few  weeks  some  wasting  of  the  face  may  be  noted,  but  this  is 
never  very  great. 

In  some  cases  there  is  with  the  paralysis  a  great  deal  of  pain  in 
and  about  the  ear  and  an  herpetic  eruption  on  the  ear,  which  may  be 
very  slight  in  amount.     A  slight  anaesthesia  of  the  concha  and  posterior 


112  DISEASES    OF    THE    NERVOUS    SYSTEM 

wall  of  the  external  meatus  is  noted.  In  these  cases,  the  trouble  is 
due  to  an  inflammation  of  the  geniculate  ganglion  which  has  extended 
and  affected  the  facial  nerve  and  the  primary  trouble  is  an  herpetic 
inflammation  of  the  ganglion  (J.  R.  Hunt). 

The  electrical  reactions  are  characteristic  and  important,  since 
typical  or  partial  degeneration  reactions  can  usually  be  observed.  For 
a  few  days  there  is  an  increase  in  irritability  of  the  muscles  to  both 
faradic  and  galvanic  currents.  This  is  followed  by  a  gradual  loss  or 
diminution  in  faradic  irritability,  while  the  galvanic  irritability  remains 
sometimes  increased  for  a  while  and  then  falls.  At  the  same  time  a 
reversal  of  poles  and  a  sluggish  contraction,  particularly  the  latter,  may 
be  noted.  At  the  end  of  five  or  six  weeks  faradic  irritability  ought  to 
begin  to  return.  Great  variations  are  found  in  the  electrical  reactions, 
dependent  upon  the  severity  of  the  case.  For  example,  in  very  severe 
cases  the  electrical  irritability  may  be  almost  or  entirely  absent  for  days 
and  even  weeks. 

If  the  disease  lasts  for  two  months  or  more  and  the  palsy  is  not  a 
complete  one,  secondary  contractures  begin  to  appear.  The  mouth 
now  becomes  drawn  to  the  affected  side,  and  the  nasolabial  fold  becomes 
deeper  than  that  on  the  sound  side.  In  smiling  or  speaking  or  other 
facial  movements  there  is  an  excess  of  movement  on  the  paralyzed  side, 
the  teeth  and  upper  gums  in  particular  showing  abnormally.  This  is 
particularly  the  case  in  old  palsies  beginning  in  childhood. 

Pathology. — The  disease  in  its  typical  form  is  due  to  a  diffuse  neuritis. 
This  attacks  the  periphery  of  the  nerve  in  the  face  and  extends  rapidly 
up  into  the  Fallopian  canal  as  far  as  the  geniculate  ganglion.  The  in- 
flammation sometimes  attacks  most  the  peripheral  filaments;  at  other 
times  it  is  more  central. 

Clark  has  recently  brought  evidence  to  show  that  the  old  idea  of  a 
"Fallopian  neuritis,"  pinching  the  nerve  and  cutting  it  off  in  the  canal, 
is  the  correct  one. 

As  already  stated,  Dr.  Hunt  has  shown  that  some  cases  of  facial 
palsy  are  due  to  the  extension  of  an  inflammation  of  the  geniculate 
ganglion,  which  is  the  sensory  ganglion  of  the  seventh  nerve. 

Bell's  palsy  is  not  a  "rheumatic"  disease;  it  is  an  infection,  and  should 
be  classed  as  such.  Many  cases  occur  after  influenza  or  some  malady 
allied  to  it.  A  long  list  of  acute  infections  which  are  occasionally  followed 
by  BelFs  palsy  may  be  collected,  but  in  the  great  majority  of  cases  it  is 
much  like  a  "cold"  of  the  seventh  nerve. 

This  view  is  borne  out  by  experience  in  treatment  which  shows  that 
antirheumatic  drugs,  like  the  salicylates  and  iodides,  do  not  appreciably 
modify  its  course. 


MOTOR  DISORDERS  OF  CRANIAL  NERVES  113 

Diagnosis. — The  recognition  of  the  palsy  is  made  easy  by  causing 
the  patient  to  contort  the  face.  In  children  it  requires  more  care  to 
detect  the  side  affected. 

It  is  important  to  determine  whether  the  pals}^  is  cerebral,  nuclear, 
basilar,  or  peripheral. 

There  is  a.  difference  in  the  grouping  of  symptoms  in  accordance  with 
the  location  of  the  lesion. 

1.  When  the  lesion  is  supra-nuclear,  that  is  between  the  cortex  and 
the  nucleus  of  the  seventh,  the  paralysis  of  the  face  involves  only  the 
lower  or  cervico-facial  branches,  and  the  patient  is  able  to  close  the 
eyes,  elevate  the  eyebrows  and  wrinkle  the  forehead.  There  are  no 
electrical  reactions  of  degeneration. 

2.  When  the  lesion  is  in  the  nucleus  itself,  there  is  very  apt  to  be  an 
associated  paralysis  of  the  sixth  nerve  on  account  of  its  close  anatomical 
relations.     Taste  and  hearing  are  unaffected. 

3.  When  the  lesion  is  at  the  exit  of  the  nerve  from  the  pons,  central 
to  the  geniculate  ganglion,  there  is  a  typical  facial  paralj^sis  without 
affection  of  taste;  but  as  such  a  lesion  implicates  usually  the  auditory 
nerve,  there  is  usually  deafness.  The  stapedius  is  paralyzed,  and  if  the 
auditory  nerve  is  injured  some  disturbance  in  hearing  may  result,  and 
there  may  be  disturbance  of  tear  secretion  on  the  paralyzed  side. 

4.  If  the  lesion  is  within  the  aqueduct  of  Fallopius  between  the  genicu- 
late ganglion  and  the  point  where  the  chorda  tympani  leaves  the  nerve, 
there  is  loss  of  taste  on  the  anterior  two-thirds  of  the  tongue  on  the 
affected  side  and  sometimes  disturbance  in  the  secretion  of  saliva. 
This  may  cause  a  furring  of  the  tongue  on  this  side. 

5.  If  the  lesion  is  far  enough  up  in  the  canal  to  involve  the  stapedius, 
there  is  sometimes  great  sensitiveness  to  loud  sounds,  or  sometimes  to 
low  sounds.  (This  sjanptom  is  much  rarer  in  the  breach  than  in  the 
observance.)  The  patient  cannot  produce  the  peculiar  sound  caused 
by  blowing  out  the  cheek  and  forcing  air  into  the  ear. 

6.  If  the  lesion  affects  the  facial  nerve  at  a  point  peripherally  to  its 
exit  from  the  stylo-hyoid  foramen,  we  have  a  complete  paralysis  of  the 
muscles  of  the  face,  but  there  are  none  of  the  disturbances  of  secretion  or 
taste  or  lachrymation  or  hearing. 

Practically  Bell's  palsy  of  the  ordinary  type  involves  portions  4, 
5,  or  6.  If  central,  the  disease  is  usually  of  syphilitic  or  tuberculous 
origin;  the  palsy  is  severe  and  the  loss  of  ability  to  close  the  eye  very 
great.  In  the  geniculate  ganglion  cases  there  is  usually  herpes,  great 
pain  and  a  slight  cutaneous  anaesthesia,  as  described.  (Hunt's  Syn- 
drome.) 

Prognosis. — The  prognosis  of  peripheral  palsy  (Bell's)  is  good, 
although  an  absolutely  complete  recovery  often  does  not  take  place. 


114 


DISEASES    OF   THE    NERVOUS   SYSTEM 


In  syphilitic  cases  the  prognosis  is  not  so  good,  though  patients  may 
recover.  In  supra-nuclear  (central)  palsies  the  prognosis  is  the  worst, 
because  the  lesion  (hemorrhage,  softening,  tumor,  etc.)  usually  does  not 
disappear. 

However,  the  central  cases  are  from  the  beginning  of  a  mild  type, 
and  give  annoyance  mainly  from  the  secondary  contractures. 

Bell's  palsy  usually  lasts  three  to  five  months.  Occasionally  there 
are  mild  cases  that  get  well  within  a  month.  The  prognosis  as  to 
duration  is  much  helped  by  a  close  study  of  the  electrical  reactions. 
In  proportion  as  the  degeneration  reaction  is  complete  and  persistent, 
the  outlook  is  bad. 


[vagus] 


Fig.  51. 


XII. 
[hypoglossal] 


-Section  of  medulla  showing  origin  of  ninth,    tenth  and  twelfth 
cranial  nerves.     {Cunningham.) 


Treatment. — In  the  acute  peripheral  cases  the  patient  should  be 
treated  promptly  and  thoroughly.  He  should  be  given  a  diuretic  and 
purgative  and  a  blister  should  be  placed  over  the  exit  of  the  nerve.  This 
should  be  followed  or  accompanied  by  hot  fomentations.  Salicylate  of 
soda  in  full  doses  of  20  grains  may  be  given  during  the  first  week. 
After  the  paralysis  is  established,  iodide  of  potassium  is  indicated  in 
moderate  doses.  Electricity  is  to  be  employed  with  care  at  first.  After 
a  week  it  may  be  given  daily  for  five  minutes,  using  the  galvanic  cur- 
rents just  strong  enough  to  contract  the  muscles.  After  three  or  four 
weeks,  if  the  faradic  current  causes  contraction  it  may  be  used,  other- 
wise the  galvanic  current  is  to  be  continued. 

At  the  end  of  three  weeks,  if  the  paralysis  is  severe,  the  corner  of  the 
mouth  should  he  drawn  up  by  means  of  a  bent  hook,  which  is  carried  back 


MOTOR  DISORDERS  OF  CRANIAL  NERVES 


115 


and  fastened  behind  the  ear.  The  patient  should  wear  this  most  of  the 
daytime,  but  not  at  night.  The  object  is  to  take  off  the  strain  caused  by 
the  pulHng  of  the  muscles  on  the  sound  side. 

At  the  end  of  a  couple  of  weeks  massage  should  be  given,  and  the 
patient  should  practice  facial  gymnastics  daily.  If  the  eye  cannot  be 
closed  it  should  be  protected  by  a  shade.  In  obstinate  cases  good  re- 
sults have  been  obtained  by  suturing 
part  of  the  hypoglossal  nerve  to  the 
facial. 


THE  GLOSSOPHARYNGEAL  NERVE 

Anatomy. — The  glossopharyngeal  nerve  has 
motor,  sensory  and  autonomic  fibres.  Its 
motor  function  is  -very  slight,  supplying  only 
the  stylo-pharyngeus. 

The  nucleus  of  origin  of  the  motor  fibres  is 
the  nucleus  ambiguus  common  to  it  and  the 
vagus  and  accessory.  The  sensory  fibres  arise 
from  two  small  ganglia  lying  on  the  root  of  the 
nerve,  the  'petrous  and  jugular. 

The  nerve  supplies  general  sensation  to 
the  tympanum,  tonsils  and  pharynx  (in  con- 
nection with  the  vagus)  and  upper  part  of 
the  larynx;  special  sensation  of  taste  to  the 
posterior  third  of  the  tongue,  and  motion  to 
the  pharyngeal  muscles  and  oesophagus 
(Kriedl)  in  connection  with  the  vagus. 

The  terminal  filaments  of  the  sensory  taste 
fibres  supplying  the  posterior  two-thirds  of 
the  tongue  end  in  fine  fibres  that  pass  into  the 
taste  buds.  There  are  no  special  peripheral 
cells  of  taste,  as  asserted  by  Fusair  and  Panasci. 

Its  cortical  representation  so  far  as  taste  is  concerned  is  in  the  hippocampal 
gyrus.  The  nerve  gives  very  sensitive  reflex  fibres  to  the  pharynx  and  is  important 
in  the  reflex  act  of  deglutition;  it  also  carries  sensations  of  nausea  from  pharyngeal 
irritation. 


Fig.  52. — -Vagus  and  spinal  acces- 
sory nerves.      {Cunjiingharn.) 


MOTOR  NEUROSES  OF  THE  GLOSSOPHARYNGEAL 


This  nerve  has  very  little  motor  function  and  is  rarely  affected 
independently  by  motor  troubles.  Spasm  of  the  pharyngeal  constrictors 
occurs  in  general  disorders  like  rabies,  and  reflexly  in  severe  neuralgia 
of  the  trigeminus.  This  condition,  known  as  dysphagia,  is  seen  also  in 
hysteria,  and  there  is  probably  sometimes  spasm  in  connection  with  the 
symptom  known  as  globus  hystericus. 

Paralysis  of  the  throat  constrictors  occurs  as  one  of  the  symptoms 
of  glosso-labio-laryngeal  paralysis  and  sometimes  in  diphtheritic  paralyses. 


116  DISEASES    OF    THE    NERVOUS    SYSTEM 

THE    PNEUMOGASTRIC    NERVE    AND    THE    ACCESSORY    PART    OF    THE 

SPINAL  ACCESSORY 

Anatomy. — The  pneumogastric  or  vagus  nerve  belongs  to  the  autonomic  nervous 
system.     It  has  two  nuclei  of  origin,  a  motor  and  a  sensory. 

1.  The  motor  nucleus  or  nucleus  ambiguus,  which  is  a  prolongation  of  the  lateral 
horn  of  the  spinal  cord  lies  deep  in  the  medulla  and  has  a  nucleus  common  to  the 
vagus  and  glossopharyngeal  (Fig.  51). 

2.  The  sensory  fibres  arise  chiefly  from  two  ganglia  that  lie  on  the  root  of  the 
nerve,  the  jugular  and  plexiform.  These  bodies  resemble  spinal  ganglia.  The 
cells  are  unipolar  and  send  off  a  neuraxon  which  bifurcates.  The  peripheral  fibre 
passes  on  along  the  nerve  and  supplies  it  with  its  sensory  fibres.  The  central  part 
passes  up  to  the  gray  matter  of  the  floor  of  the  fourth  ventricle  and  ends  in  the  so- 
called  sensory  nucleus  (Fig.  47).  This  nucleus,  however,  is  not  the  real  nucleus  of 
origin,  but,  as  in  the  case  of  the  ninth,  it  contains  cells  which  send  their  axis-cylinders 
or  neuraxons  brainward  and  form  secondary  sensory  neurons.  Fibres  also  go  to  the 
ascending  sensory  root  common  to  this  nerve  and  the  ninth. 

The  spinal  accessory  nerve  is  purely  motor  in  function  (Van  Gehuchten).  The 
accessory  part  arises  from  the  cells  of  the  nucleus  ambiguus  and  passes  into  the 
trunk  of  the  vagus. 

The  spinal  part  of  the  spinal  accessory  arises  from  the  lateral  horn  and  outer  part 
of  the  anterior  horn  of  the  spinal  cord.  Its  fibres  of  orign  reach  from  the  first  to  the 
third  or  fourth  cervical  nerves  and  as  far  as  the  fourth  or  fifth  cervical  roots.  The 
fibres  unite  in  the  cranium  and  pass  out  through  the  posterior  lacerated  foramen  in 
the  same  sheaths  as  the  vagus.  After  their  exit  from  the  skull,  they  divide  into  an 
internal  and  external  part.  It  is  the  external  branch  which  contains  the  fibres  of 
spinal  origin.  The  internal  part  contains  the  fibres  from  the  medulla  and  unites 
with  the  vagus.  The  nerve  receives  some  sensory  fibres  from  the  first  and  some- 
times from  the  second  cervical  nerve.  The  terminal  branches  receive  motor  fibres 
from  several  cervical  nerves.  The  spinal  accessory  contains  large  and  small  or 
visceral  fibres.     The  spinal  part  contains  only  the  large  fibres. 

The  spinal  accessory  supplies  the  sterno-cleido-mastoid  almost  exclusively,  but 
only  the  upper  part  of  the  trapezius;  the  rest  of  this  muscle  is  supplied  by  the  cervical 
and  dorsal  nerves.  The  sterno-cleido-mastoid,  when  innervated,  draws  the  chin  up 
and  over  toward  the  opposite  side.  The  upper  fibres  of  the  trapezius  draw  the  head 
back  slightly  and  down  toward  the  same  side.  Physiologically,  the  spinal  part  of 
the  accessory  nerve  is  one  of  the  motor  cervical  nerves;  the  accessory  or  medullary 
portion  is  part  of  the  vagus,  and  has  visceral  and  sensory  as  well  as  motor  functions.' 

The  vagus  and  accessorj"-  part  of  the  eleventh  together  have  an  extraordinary 
wide  distribution  and  diversity  of  function. 

1.  First  they  contain  motor,  inhibitory,  and  vasomotor  fibres.  These  fibres  go 
to  the  pharynx,  larynx,  trachea  and  bronchi,  to  the  oesophagus,  stomach,  small 
intestines  and  spleen. 

2.  Sensory  fibres,  which  go  the  occipital  and  transverse  sinuses  and  dura  mater 
of  the  posterior  fossa,  to  the  external  auditory  meatus  in  part,  to  the  pharynx,  larynx 
and  trachea  and  to  the  oesophagus. 

3.  Excito-reflex  fibres,  which  go  to  the  lungs  and  heart,  stomach,  and  to  other 
organs  mentioned  as  supplied  by  the  vagus  with  sensation. 

These  reflex  fibres  stimulate  or  inhibit  the  vasomotor  centre,  the  respiratory 
rhythm  and  the  cardiac  rhythm.  They  also  excite  reflexly  deglutition  and  re- 
spiratory movements. 

^  The  special  autonomic  character  of  the  vagus  has  been  noted  under  the  head  of 
the  sympathetic  nervous  system. 


MOTOR  DISORDERS  OF  CRANIAL  NERVES  117 

The  secretory  fibres  go  to  the  respiratory  tract,  oesophagus,  stomach  and  pancreas 
and  small  intestines. 

Cardio-inhibitory  fibres  go  to  the  heart,  while  reflex  accelerating  fibres  and  in- 
hibiting fibres  go  to  the  lungs.  The  accessory  nucleus  supplies  the  laryngeal  adductors 
and  the  cardio-inhibitory  fibres. 

DISEASES  OF  THE  VAGUS— ACCESORY    NERVES— VAGOTONIA 

These  nerves  are  essentially  autonomic  in  character.  Their  diseases 
call  for  a  study  of  laryngeal,  pulmonary,  cardiac  and  abdominal  neu- 
roses, which  would  bring  us  into  the  domain  of  laryngology  and  general 
medicine.  Hence,  despite  their  great  importance,  I  have  thought  it 
best  to  describe  only  a  special  neurosis  due  to  functional  vagus  dis- 
turbance and  in  a  general  way,  the  anatomical  supply  and  function  of 
the  laryngeal  nerves.  Some  of  the  other  symptoms  of  its  disorders  are 
described  in  connection  with  locomotor  ataxia,  progressive  muscular 
atrophy,  exophthalmic  goitre,  and  angina  pectoris. 

VAGOTONIA 

There  has  been,  however,  an  attempt  of  late  to  show  that  sometimes 
the  pneumogastric  nerve  is  thrown  into  acute  tonus  or  stimulation,  often 
in  association  with  other  cerebral  autonomic  nerves.  This  condition 
is  called  vagotonia. 

Eppinger,  Hess  and  others  have  worked  out  a  neurosis  of  the  cerebral 
autonomic  system. 

In  a  typical  vagotonic  attack  all  or  nearly  all  of  the  cerebral  au- 
tonomic nerves  are  affected.  As  the  result,  there  is  narrowing  of  the  pupil 
from  irritation  of  the  ciliary  ganglion  (III  nerve),  salivation  and  flow  of 
tears,  from  irritation  of  the  chorda  tympani  and  lachrymal  nerve  (VII 
nerve),  hyperidrosis  from  irritation  of  the  cervical  sympathetic,  brady- 
cardia and  respiratory  arythmia,  bronchial  asthma,  hyperacidity  and 
increased  gastric  motility,  from  irritation  of  the  vagus. 

This  group  of  symptoms  has  this  in  common,  that  all  are  alleviated 
by  large  doses  of  atropia,  and  all  are  increased  by  pilocarpin.  It  is  a 
clinical  picture  built  up  more  on  pharmacological  than  clinical  data. 
I  think  we  see  only  the  fragments  of  it. 

A  commoner  form  of  vagotonia,  it  seems  to  me,  shows  itself  as  a  real 
clinical  phenomenon  much  more  frequently  in  what  Gowers  has  described 
as  vagal  and  vaso-vagal  attacks.  These  are  characterized  by  subjective 
or  sensory  disturbances  mainly.  The  patient,  for  example,  first  feels  a 
sensation  of  distress  or  distention  of  the  stomach,  which  may  be  asso- 
ciated even  with  nausea  and  faintness.  With  it  there  comes  a  feeling  of 
respiratory  distress  and  inability  to  get  the  breath,  a  feeling  of  impending 
death  or  a  sensation  of  fainting.  There  is  generally  a  rather  slow  pulse 
and  cold  extremities.     Occasionally  the  patient  feels  a  very  heavy  beat- 


118  DISEASES    OF    THE    NERVOUS    SYSTEM 

ing  of  the  heart.  There  is  flatulence,  and  when  gas  is  raised  the  symptoms 
are  relieved  in  part.  The  stomach  shows  increased  acidity  and  evidence 
of  excessive  motility  or  spasm. 

There  is  a  mental  condition  of  confusion  and  alarm,  and  this  often 
simulates  hysteria,  and  these  vagal  seizures  are  often  regarded  as 
hysterical. 

The  Laryngeal  Nerve-supply. — Phonation  is  mostly  a  voluntary  act, 
and  has  a  centre  in  the  cortex  of  both  hemispheres  at  the  lowest  level 
of  the  prsecentral  convolution.  By  its  stimulation  adduction  of  the 
vocal  chords  can  be  produced. 

Respiratory  movement  (abduction  of  the  vocal  chords)  has  no  cortical 
centre.     Its  centre  is  in  the  medulla  near  the  vagal  nuclei. 

The  motor  nerve  of  the  larynx  is  the  recurrent  laryngeal  which  inner- 
vates all  the  muscles,  adductor  as  well  as  abductor,  except  the  cricothyroid 
which  is  innervated  by  the  superior  laryngeal. 

The  motor  fibres  for  the  abductors  (respiratory  fibres)  run  in  a  separate 
bundle  inside  the  recurrent  nerve  while  the  adductor  or  phonatory  fibres 
run  on  the  outer  part  (R.  Russell). 

The  abductors  are  paralyzed  first  and  most  easily  and  are  especially 
apt  to  be  affected  by  progressive  organic  disease  in  the  bulb. 

But  in  functional  diseases  (psychic,  hysterical)  the  adductors  are 
exclusively  affected.  This  is  because  the  impulses  to  the  adductor 
muscles  have  a  wider  range  of  fibres  to  work  upon.  When  there  is 
complete  recurrent  nerve  palsy,  the  vocal  chord  is  motionless  and  in 
a  position  near  the  median  line. 

The  superior  laryngeal  is  the  sensory  nerve  of  the  larynx,  and  when 
it  is  injured  there  is  anaesthesia  of  the  larynx  and  paralysis  of  the  crico- 
thyroid which  is  a  tensor  muscle. 

In  vagus  paralysis  high  up  on  one  side  we  have  anaesthesia  of  the 
larynx  with  loss  of  reflex  phenomena  and  consequent  passage  of  foreign 
bodies,  food,  etc.,  into  the  larynx;  also  tachycardia  and  paralysis  of 
the  abductors,  which  may  be  bilateral. 

In  paralysis  of  the  superior  laryngeal  we  have  only  the  anaesthesia 
of  the  larynx  with  its  resulting  loss  of  reflex  protective  activity. 

In  paralysis  of  the  recurrent  laryngeal  we  may  have  at  first  and 
only  abductor  paralysis,  later  total  paralysis  of  the  vocal  cord. 

The  causes  are  injuries,  infectious  and  degenerative  diseases,  such 
as  tabes,  syphilis,  progressive  bulbar  palsy,  and  any  organic  bulbar 
lesions,  such  as  tumors,  hemorrhage  and  softenings.  The  recurrent 
laryngeal  suffers  sometimes  from  what  is  probably  an  infectious  neuritis, 
causing  subacute  paralysis  of  one  abductor  which  is  recoverable.  The 
commonly  observed  cause  is  aneurism  of  the  aorta  and  tumors  of  the 
mediastinum  or  neck,  such  as  goitre. 


MOTOR    DISORDERS    OF    CRANIAL    NERVES  119 

NEUROSES   OF   THE   SPINAL   PART   OF   THE  ACCESSORIUS   AND   UPPER 

CERVICAL  NERVES 

The  accessory  is  a  purely  motor  nerve,  and  its  disorders  are  there- 
fore spasm  and  paralysis. 

Torticollis  (Wry-neck,  Caput  Ohstipum). — Torticollis  is  a  disease 
characterized  by  clonic  or  tonic  spasm  of  the  muscles  supplied  by  the 
spinal  accessory  and  often  of  other  muscles  of  the  neck.  There  are 
several  forms  of  wry-neck,  which  must  be  distinguished  from  each  other. 
They  are:  (1)  congenital  wry-neck;  (2)  symptomatic  wry-neck;  (3)  spurious 
wry-neck,  from  spinal  disease;  (4)  true  spasmodic  wry-neck. 

1.  Congenital  wry-neck  is  due  to  some  intra-uterine  atrophy  or  ob- 
stetrical injury  of  the  sterno-cleido-mastoid.     It  occurs  oftenest  after 


Fig.  53. — Congenital  wryneck  of  the  right  side. 

breech  or  foot  presentations.  The  right  side  is  usually  affected.  There 
is  no  spasm  at  all,  but  the  neck  is  fixed  to  one  side  by  the  shortness  of 
the  muscle,  and  also  rotated  to  the  opposite  side.  The  deformity  be- 
comes more  noticeable  as  the  child  grows  older,  because  the  parts  atrophy. 
The  atrophy  affects  not  only  the  shortened  muscles,  but  the  face  on  the 
affected  side  (Fig.  53). 

2.  Symptomatic  wry-neck  is  usually  due  to  a  rheumatic  myositis,  and 
occurs  chiefly  in  children.  It  may  be  due  also  to  tumors,  adenitis,  ab- 
scesses and  local  syphilitic  disease.  In  these  cases  there  are  always  pain 
and  tenderness  associated  with  the  deformity. 

3.  Spurious  wry-neck  is  an  apparent  or  real  spasm  of  the  neck  muscles 
due  to  caries  of  the  spine.  A  spurious  wry-neck  may  be  caused  by  defect 
of  the  oculo-motor  apparatus  such  as  lateral  nystagmus  (Starr). 

Treatment. — Congenital  wry-neck,  if  taken  early,  can  be  cured  by 
tenotomy   of  the  sterno-mastoid  and  subsequent  fixation    of  the  neck 


120 


DISEASES    OF    THE    NERVOUS    SYSTEM 


for  a  time.  When  osseous  changes  have  occurred  perfect  rehef  is  im- 
possible. Symptomatic  rheumatic  wry-neck  is  a  trivial  and  temporary 
affection,  which  needs  only  to  be  palliated  by  hot  applications,  saUcylates 
and  saline  purges  until  cure  takes  place. 

Spurious  wry-neck  requires  suitable  orthopaedic  measures,  such  as 
the  plaster  jacket  and  jurymast. 

4.  Spasmodic  Wry-neck. — This  is  a  purely  nervous  disease  charac- 
terized by  spasm  of  the  muscles  supplied  by  the  spinal  accessory  and 
generally  of  those  supplied  by  the  upper  cervical  nerves  also. 

Etiology. — Women  are  oftener  affected  than  men.  It  arises  in 
early  adult  and  middle  life,  never  in  children  or  old  people.     The  sufferers 


Fig.  54. 


-Typical  wryneck  involving  the  spinal  accessory  on  the  right 
side.     (Walton.) 


are  of  a  neuropathic  constitution  and  direct  heredity  may  exist.  Over- 
work and  exhausting  emotions  are  apparent  predisposing  causes. 

The  exciting  causes  are  occupations  which  put  the  lateral  muscles  of 
the  neck  on  a  strain,  or  in  which  frequent  lateral^movements  of  the  head 
have  to  be  made.     It  is  then  an  occupational  neurosis  like  writer's  cramp. 

Trauma,  peripheral  irritation,  eye-disease,  various  infections  and 
toxsemic  states  which  depress,  may  excite  the  disease  in  a  neuropathic 
person. 

Symptoms. — The  disease  begins  with  slightly  painful  sensations  in 
the  neck,  which  are  soon  accompanied  by  spasm.  The  spasm  is  at 
first  clonic  and  intermittent.  The  sterno-mastoid  is  oftenest  involved 
of  single  muscles,  but  the  rule  is  that  the  upper  fibres  of  the  trape- 
zius are  also  affected.  The  patient's  head  is  inchned  toward  the  affected 
side  by  the  trapezius,  the  chin  is  raised,  and  the  head  rotated  to  the 
opposite  side  by  the  sterno-mastoid  and  trapezius,  and  this  is  the  typical 
position  in  the  disease  (Fig.  54).     If  both  trapezii  are  affected  the  head 


MOTOR  DISORDERS  OF  CRANIAL  NERVES 


121 


is  pulled  back,  but  this  is  a  rare  form.  It  is  called  retro-collic  spasm. 
The  complexus  and  obliquus  superior  are  the  only  other  neck  muscles 
which  can  rotate  the  head  to  the  opposite  side.  They  are  supplied 
by  the  upper  cervical  nerves  and  are  often  involved  in  wry-neck.  In 
torticollis  the  muscles  affected  with  spasm  have  a  similar  physiological 
function.  Hence,  while  the  sterno-mastoid,  trapezius,  complexus  and 
superior  oblique  on  one  side  are  attacked  by  the  spasms,  muscles  on  the 
other  side  may  be  at  the  same  time  implicated.  The  opposite  muscle 
commonly  affected  is  the  splenius,  which  inclines  the  head  laterally  and 
rotates  it  to  the  same  side.  Probably  the  deep  muscles,  recti  capitis 
postici,  major  and  minor,  and  the  inferior  oblique,  which  draw  the  head 
back  and  rotate  to  the  same  side,  are  also  at  times  affected.  The  list 
of  muscles  that  may  be  involved  and  their  nerve  supply  are  as  follows: 


Turning  head  to  Opposite  Side  1    "^^^^"^ '^a^'sid^  ^^^"^     ^^^^'^  ^^^PP'^ 

i 

Muscles  usually  in- 
volved 

Sterno-cleido-mastoid. . .  . 

Eleventh. 

Upper  fibres  of  trapezius. 

Eleventh. 

Muscles   rarely  in- 
volved 

Superior  obliquus 

Complexus 

Recti  capitis  postici,  maj., 
miri.,        infer.        obliq., 
splenius. 

Cervical. 
Cervical. 

Extreme  rotation  without  much  retraction  of  the  head  would  indicate 
involvement  of  the  sterno-cleido-mastoid  and  opposite  splenius.  Re- 
traction of  the  head  indicates  involvement  of  both  trapezii  or  the  deep 
recti  muscles.  A  full  account  of  the  physiology  of  the  neck  muscles  is 
given  later  under  the  motor  neuroses  of  the  upper  cervical  nerves — where 
torticollis  more  properly  belongs. 

The  disease  may  start  in  one  muscle  and  gradually  extend  to  others, 
even  involving  the  facial,  masticatory  and  brachial  nerves.  As  it 
progresses  the  spasm  becomes  more  constant,  and  finally  it  may  be 
tonic,  never  yielding  except  to  artificial  means  or  during  sleep.  The 
pain  associated  with  the  disease  gradually  decreases.  The  affected 
muscles  hypertrophy,  the  muscles  thrown  into  disuse  atrophy.  There 
is  some  deformity,  in  time,  of  the  neck  and  shoulders,  but  facial  asym- 
metry does  not  occur  in  this  form  unless  it  begins,  as  is  very  rarely  the 
case,  before  maturity. 

The  disease  reaches  a  chronic  stage  in  one-half  a  year  to  a  year, 
then  remains  stationary  or  gradually  improves.  The  disease  may  be 
complicated  with  other  neuroses  or  a  psychosis. 

Pathology. — -TorticolHs  is  a  psycho-neurosis  involving  the  bulbar  and 
lower  psychic  centres.     The  disease  is  in  its  usual  form  a  degenerative 


122  DISEASES    OF    THE    NERVOUS    SYSTEM 

one,  and  indicates  the  premature  decay  or  exhaustion  of  centres  never 
perhaps  originally  perfect.  It  is  called  in  its  typical  form  by  French 
writers  "mental  torticollis."  But  all  true  torticollis  is  "mental,"  in 
the  sense  that  the  normal  volitional  control  is  lost  and  the  psychic  part 
of  the  mechanism  is  disturbed.  It  is  not  '^ mental"  in  the  sense  that  it 
is  dependent  on  an  idea,  except  in  cases  occurring  in  early  life  when  it 
may  be  psychogenic. 

The  diagnosis  has  to  be  made  from  the  other  forms  of  wry-neck  men- 
tioned. The  age,  history  and  fixed  character  of  the  spasm  serve  to 
distinguish  congenital  wry-neck.  The  history,  the  pain  and  tender- 
ness and  the  temporary  duration  differentiate  the  rheumatic  forms. 

The  increased  rigidity  on  passive  motion,  the  pain,  deformity,  and 
other  signs  of  cervical  caries  are  sufficient  to  diagnosticate  vertebral 
disease. 

Prognosis. — The  disease  is  not  fatal.  It  generally  reaches  a  certain 
stage  and  then  remains  chronic.  In  young  and  psychogenic  cases  it  is 
cured;  in  many  others  it  can  be  much  ameliorated. 

Treatment. — The  drugs  which  are  useful  are  very  few.  Opium, 
chloral,  atropin,  the  bromides,  and  zinc  are  generally  the  most  efficacious. 
Opium  must  be  given  with  great  caution.  Atropin  should  be  given 
hypodermically  in  increasing  doses  up  to  intoxication  (gr.  ^f  o)  (Les- 
zynsky).  The  galvanic  and  faradic  currents  are  useful  adjuvants  in  help- 
ing to  relax  the  spasm  and  keep  up  the  nutrition  of  the  muscles,  but  alone 
they  are  of  little  value.  Massage  and  stretching  the  neck  in  a  Sayre 
apparatus,  together  with  systematic  exercise  of  the  neck  muscles,  often 
help.  The  only  surgical  measures  to  be  advised  are  nerve  resection, 
and  possibly  the  partial  cutting  of  the  sterno-mastoid  muscle. 

The  pedagogical  and  psycho-therapeutic  method  of  dealing  with  torti- 
collis, by  rest,  massage,  exercises  and  relaxation,  is  the  most  important 
of  all  measures.  This  form  of  treatment  must  be  combined  with  rest, 
tonics  and  symptomatic  remedies,  and  it  must  be  begun  if  possible  early 
and  kept  at  persistently  and  repeatedly — ^if  necessary  even  for  two  or 
three  years.  Prolonged  rest  for  months  or  even  much  longer  with 
pedagogical,  local  and  general  exercises  are  the  basis  of  rational  treat- 
ment and  often  of  practical  cure. 

Psycho-analysis  and  hypnotism  do  no  good,  except  perhaps  in  young 
and  distinctly  hysterical  patients. 

Splints  and  mechanical-fixation  apparatus  do  no  good,  as  a  rule. 
Alcoholic  injections  may  be  tried.  I  have  never  seen  permanent  good 
from  surgery. 

Paralysis  of  the  Spinal  Part  of  the  Accessory — Etiology. — The  chief 
causes  are  injuries,  caries  of  vertebra,  progressive  muscular  atrophy, 
and  anterior  poliomyelitis. 


MOTOK  DISORDERS  OF  CRANIAL  NERVES  123 

Symptoms. — When  one  nerve  is  paralyzed  the  head  may  still  be  held 
straight,  but  there  is  inability  to  rotate  it  perfectly.  The  prominence  of 
the  sterno-mastoid  is  absent — ^atrophy  takes  place.  No  spasm  of  the 
other  muscle  occurs,  and  there  is  no  such  thing  as  paralytic  torticollis 
(G'owers).  The  involvement  of  the  trapezius  causes  a  depression  in  the 
contour  of  the  neck,  especially  noticeable  on  deep  inspiration.  There  is 
some  trouble  in  raising  the  arm,  the  scapula  is  drawn  away  from  the 
spine,  and  the  lower  angle  is  rotated  inward.  When  both  nerves  are 
paralyzed  there  is  great  difficulty  in  rotating  the  head  or  raising  the 
chin.  Paralysis  of  both  sterno-mastoids  causes  the  chin  to  drop  back- 
ward, while  paralysis  of  both  trapezii  in  their  upper  parts  causes  the  head 
to  drop  forward.  Atrophy  of  the  muscles  attends  the  paralysis  of  the 
nerve,  and  degenerative  reactions  may  be  noted.  The  cervical  nerves 
appear  sometimes  to  supply  the  sterno-mastoid  and  upper  part  of  the 
trapezius  so  much  that  in  disease  of  the  accessories  decided  paralytic 
symptoms  may  be  absent. 

The  diagnosis  depends  upon  a  thorough  examination  of  the  motility 
of  the  parts. 

The  treatment  is  based  on  a  knowledge  of  the  cause  of  the  disease. 

THE  HYPO  GLOSSUS— XII 

Anatomy. — -The  hypoglossal  nerve  arises  from  a  long  and  large  nucleus  lying  on 
the  lower  part  of  the  floor  of  the  medulla  near  the  median  line  and  to  the  outer  and 
ventral  side  of  the  central  canal.  The  nucleus  is  a  continuation  upward  of  the 
anterior  horns  of  the  spinal  cord  and  is  homologous  with  the  sixth,  fourth  and  third 
nerve  nuclei  higher  up  (see  Fig.  47).  It  reaches  below  as  far  as  the  decussation  of 
the  pyramids  and  above  as  far  as  the  glosso-pharyngeal  nucleus.  A  second  small- 
celled  nucleus  lies  just  beneath  the  nucleus  proper.  Its  cortical  representation  is  in  the 
lower  end  of  the  prsecentral  convolutions,  to  which  it  is  connected  by  fibres  that  pass 
into  the  raphe  and  thence  to  the  anterior  pyramids.  Its  fibres  pass  out  between  the 
olivary  body  and  the  anterior  pyramid.  At  its  origin  it  is  a  purely  motor  nerve;  it 
receives  a  few  sensory  fibres  from  the  cervical  nerves  and  the  vagus.  It  supplies  the 
intrinsic  and  extrinsic  muscles  of  the  tongue :  It  is  also  thought  to  send  fibres  to  the 
oral  muscles  (Tooth). 

The  hypoglossal  nerve  is  concerned  in  the  movements  of  the  tongue 
and  in  fixing  or  depressing  the  hyoid  in  mastication  and  deglutition. 
When  diseased,  therefore,  speech  and  deglutition  are  affected.  The 
small  nucleus  of  the  nerve  is  thought  to  control  the  finer  lingual  move- 
ments of  articulation. 

MOTOR  NEUROSES  OF  THE  HYPOGLOSSAL  NERVE— THE  MECHANISM 

OF  ARTICULATION 

The  diseases  of  this  nerve  consist  of  lingual  spasms,  lingual  palsy  and 
lingual  hemiatrophy. 


124  DISEASES    OF   THE    NERVOUS    SYSTEM 

Lingual  spasms  take  part  in  the  disorders  of  articulation,  helping  to 
cause  stuttering  and  speech  cramps.  Such  troubles  are  often  develop- 
mental in  origin  and  belong  to  the  habit  choreas  or  convulsive  tics. 

Stuttering  is  a  spasmodic  disorder  of  the  mechanism  of  articulation, 
causing  a  habitual  and  spasmodic  repetition  of  words,  or  syllables. 

Stamynering  is  spasmodic  abortive  speech  caused,  according  to 
E.  Thompson,  by  the  effort  of  the  stammerer  consciously  to  do  what 
should,  and  must  be  done,  automatically. 


Fig.  55. — Left  lingual   hemiatrophy. 

Aphthongia  is  the  name  given  to  a  form  of  spasm  occurring  in  speakers 
and  similar  in  nature  to  writer's  cramp. 

Clonic  lingual  sx)asm  occurs  in  chorea,  hysteria  and  during  the  attacks 
of  epilepsy.  Unique  cases  of  this  spasm  also  occur  from  reflex  irritation 
or  central  nervous  disease. 

Tonic  lingual  spasm  occurs  in  hysteria,  and  sometimes  as  an  inde- 
pendent affection  due  to  local,  toxic  or  reflex  irritation. 

Lingual  paralysis  (glossoplegia)  is  usually  one  of  the  symptoms  of 
glosso-labio-laryngeal  palsy.  It  may  also  be  caused  by  a  bilateral  or 
even  a  single  lesion  in  the  cerebral  hemispheres.  The  condition  is  then 
known^  as  pseudobulbar  paralysis.  Diseases  of  the  medulla  and  of  the 
nerve  itself  may  cause  paralysis  and  atrophy.  The  paralysis  may  be 
either  unilateral   or   bilateral.     The   symptoms  are  an  impairment    of 


NERVOUS  DISEASES 

DANA 


Scheme  of  Nerve  Distribution. 

"The  segments  are  printed  in  red.    The  motor  nerves  or  portions  of  mixed  nerves  In  solid  blue 
lines.    The  sensory  nerves  or  sensory  portions  of  mixed  nerves  in  dotted  blue  lines. 


•  la)  Interior  eye  muscles  (Intercalation  of  the  ciliary  ganBllon).  ciliary  muscle  for  accommodation 
*  —sphincter  of  tlie  pupil  for  contraction  of  the  pupil.  ,     ■    r     i 

(b)  exterior   eye  muscles  j  levator  palpebree   superioris  ;   rectus   Hupenor,  internuj,    interior- 
inferior  oblique,  movement  of  the  eyeballs  upward,  inward,  and  downward. 

unerior  oblique  of  the  eye  (movement  downward  and  outward).  ^  •      *       t „„: 

lUBcles of  mastication;  masseter,  temporal,  pterygoid,  mylo-hyoid-ant.  digastric,  tensor  tympani. 
ensor  and  levator  veli  palati.    Secretion  of  tears  ? 

Ixternal  rectus  of  the  eye  (outward  movement).  ,  ,.  ..  ,  ,.1    „i„*„„„„ 

'he  Simic  face  muscles;  frontal,  orbicular  of  the  eye  and  mouth;  zygomaticl,  n^ental ;  Dlatysma 
)f  the  ears,    stapedius,    posterior  digastric,  etc.      Nasal   secretions.      Tear   secretion?     Palate 

^hroat^muTculature  (constrictors),  crico-thyroid.  secretion  of  gastric  juice.  Movements  of  heart 
'ongue  musculature,  sterno-hyoid.  thyreoidei.  f».L  S„™lt  rnit  nf 

.arynx  musculature  (voice  formation),  palate,  pharyngeal  musculature,  (with  the  vagus  (act  of 
wLlowing)-8terno  oleido-mastoid  (drawfng  the  tead  laterally  and  nodding,.  Trapezius  (in  part) 
shrugging  the  shoulders). 

>osterior  superBcial  and  deep  head  and  neck  muscles  (elevating  and  lateral  movements  of  head). 
Jeep  posterior  and  anterior  back  muscles.    Trapezius  in  part  (movement  of  head  and  throat). 

,  icaleni  (elevators  of  the  ribs,  breathing),  longus  colli. 
Diaphragm  (breathing). 

![  'IctoraUsmajortanterior  adduction  of  the  upper  arm),  pectoralis  minor,  subclavius.  „„„„., 

:.evator  scapul».  rhomboids  (dorsal  nerves  of  the  scapula)  (draws  the  scapula  inward  and  "Pwardn 
"erratus  anticus  major  (long  thoracic  nerve)  fixes  the  shoulder  blade  and  draws  the  same  in 
jonjunction  with  the  arm  above  the  horizontal. 

I  ;upraBpinatus  (raises  and  rolls  the  arm  outward),  infraspinatus,  teres  minor  (rolls  outward). 

liubscapularis.  teres  major  (rotates  inward),  latissimus  dorsi  (adducts  the  arm  and  draws  it  backward). 

I  deltoid  (raises  the  arm  to  horizontal).  „  ,,  ,  u       v  i-~ 

Biceps  iflexor  of  forearm  and  supinator!,  brachialis  anticus  (flexor  of  forearm),  coracobrachialis. 
Ulloi  communis  digitorum  (radial  portion)  (bends  the  terminal  phalanges,,  flexor  longus  Polliols 
end  phalanx),  flexo?  carpi  radialis,  pronator  radii  teres,  and  Q»adratus,  palmaris  longus,  thenar 
mSsoles  (opponents  of  thumb  flex  tte  primary  phalanges  and  extend  the  terminal  phalanges)   lum- 
bricales  1.  2.  seldom  3  (flex  the  peripheral  phalanges  and  extend  simultaneously  the  terminal 

&\!e?s^flxten8or  of  forearm),  radial  portion  of  brachialis  anticus,  supinator  longus!  (flexes  and 
prinatls  the  forearm)?  exteksor  communis  digitorum  (extensor,  of  the  peripheral,  phalanges), 
extensor  pollicis-abductor  pollicis.  supinator  brevis,  extensor  carpi  radialis  and  ulnaris.  . 

2^Flexor  profundus  digitorum  (ulnar  portion),  see  20.    Flexor  carpi  ulnaris.  hypothenar.  interossel 
(flex  the  peripheral  phalanx),  lumbrioales  (3  and  4),  see  20,  adductor  polliois. 

9 1  Deep  back  muscles. 

j  Intercostal  muscles. 

SlDeep  back  muscles  (extensor  of  trunk). 

f  Intercostal  muscles. 

i  Intercostal  muscles,  abdominal  muscles  (rectus,  external  oblique)  'compressor  of  abdomen). 

Back  (lumbar)  muscles. 

Transverse  abdominal,  internal  oblique-  (compressor  of  abdomen). 

]  Oremaster,  transverse,  oblique. 

t  External  obturator,  adductor  of  thigh,  gracilis  (adductor). 

Psoas  (lumbar  plexus),  iliacus  internus  (draws  up  the  thigh,  flexes  the  trunk),  quadriceps  (extends 
the  leg),  sartorius. 

Gluteus  medius,  minimus  (abductors  of  thigh),  tensor  vaginae  femoris,  pyriformis,  obturator 
internus  (abductors). 

Gluteus  maximus  (extends  the  thigh).  „      ,,     ,     ,  o  ,  «  ■    ,  jj   „4. > 

Gemelli ;  biceps,  semitendinosus,  semimembranosus  (flex  the  leg),  quadriceps  femoris  (adductor). 

J  Tibialis  anticus  (raises  the  inner  border  of  foot),  peronei  (raise  outer  border  of  foot),  extensot 
digiti  communis.  .  „  ,.   .i.   i.._.  i-  ^■ 

Gastrocnemius,  soleus  (plantar  flexion  of  the  foot),  flexor  digiti,  tibialis  posticus. 

I  Small  muscles  of  foot  (flexor  brevis,  interossei,  etc.). 
Levator,  internal  sphincter  ani,  sphincter  vesicae. 
Sphincter  ani,  perineal  musculature,  bulbi  cavernosi,  etc. 
External  sphincter  ani. 


MOTOR    DISORDERS    OF    CRANIAL    NERVES  125 

speech  and  of  swallowing.     Fuller  details  will  be  given  under  the  head 
of  Bulbar  Palsy. 

Progressive  Lingual  Hemiatrophy. — A  progressive  hemiatrophy  of 
the  tongue  sometimes  occurs.  It  is  analogous  in  all  respects  to  facial 
hemiatrophy,  with  which  it  is  sometimes  associated.  It  is  probably  due 
to  a  low  grade  of  degenerative  neuritis  of  the  nerve. 


CHAPTER  IX 
NEUROSES  OF  THE  MOTOR  SPINAL  NERVES 

Anatomy  and  Physiology. — ^The  spinal  nerves  arise  from  the  spinal  cord  by  two 
roots,  anterior  and  posterior.  These  roots  unite  outside  the  spinal  canal  to  form, 
mixed  nerves.  The  mixed  nerves  divide  and  go  to  their  various  destinations.  There 
are  thirty-three  pairs  of  spinal  nerves,  viz.: 

Cervical 8 

Dorsal 12 

Lumbar 5 

Sacral 5 

Coccygeal 3  (all  rudimentary). 

33. 

The  last  two  coccygeal  nerves  are  microscopic  in  size,  and  the  first  pair  is  very  small, 
so  that  practically  there  are  but  thirty  sets  of  spinal  nerves. 

The  posterior  roots  are  closely  connected  with  ganglia  lying  in  the  intevertebral 
canal,  and  called  intervertebral  gangla,  or  ganglia  of  the  posterior  roots.  These 
ganglia  are  the  real  origin  of  the  great  majority  of  the  fibres  of  these  roots.  The 
mixed  nerve  is  connected  by  fibres  that  come  chiefly  from  the  anterior  root,  with 
the  sympathetic  or  prsevertebral  ganglia.  The  distribution  of  the  spinal  nerves  is 
shown  in  Plate  III. 

For  the  purpose  of  conveniently  studying  the  diseases  of  the  spinal  nerves,  we 
divide  them  into  six  different  groups,  each  having  a  somewhat  definite  work  to  do. 
These  groups  are  shown  in  the  accompanying  table. 


Strands  of  Spinal  Nerves 


Distribution 


Associated  Ganglia  of  Sym- 
pathetic 


Group  I. 

Upper  four  cervical. 

Group  II. 

Lower    four    cervical     and 

first  dorsal. 

Group  III. 

Upper  six  dorsal. 

Group  IV. 

Lower  six  dorsal,  except  last. 

Group  V. 

Twelfth  dorsal,  four  lumbar. 

Group  VI. 

Fifth  lumbar  and  five  sacral. 

Occipital  region,  neck. 
Upper  extremities. 


Thoracic  wall. 

Abdominal  wall,  upper  lum- 
bar, upper  lateral  thigh 
surface. 

Lumbar  region,  upper  glu- 
teal, anterior  and  inner 
thigh  and  knee. 

Lower      gluteal,      posterior    First  to  fifth  sacral 
thigh,  leg,  pelvic  organs. 


First  cervical. 

Second  and  third  cervical, 

first  dorsal. 
First  to  sixth  dorsal. 
Fifth  to  twelfth  dorsal. 


First  to  fourth  lumbar. 


GROUP  I.     THE  UPPER  CERVICAL 


includes  the  first  four  of  the  spinal  nerves.     These  divide  into  anterior  and  jjosterior 
branches.     The  posterior  branches  supply  the  muscles  and  skin  of  the  back  of  the 

126 


NEUROSES    OF    THE    MOTOR    SPINAL    NERVES  127 

neck  and  the  occiput.  The  principal  nerves  are  the  suboccipital  and  the  great 
occipital. 

The  anterior  branches  form  the  cervical  plexus.  Its  principal  branches  are  the 
auricularis  magnus,  occipitals  minor,  and  phrenic.  The  special  distribution  of  the 
nerves  is  shown  in  the  table.     (See  Appendix.) 

The  upper  cervical  nerves  supply  motion  to  the  muscles  which  rotate  the  head 
and  draw  it  back  and  sideways. 

One  branch,  the  phrenic,  supplies  the  diaphragm;  others  supply  muscles  which 
assist  in  fixing  the  thorax  in  forced  inspiration.  They  innervate  some  of  the  hyoid 
and  thyroid  muscles,  but  have  no  influence  on  phonation  or  deglutition.  This  group 
of  nerves  is  in  close  connection  centrally  with  the  trigeminal  nerve,  whose  descending 
root  reaches  down  into  the  cervical  cord.  The  fibres  to  the  scalp  and  face  also 
anastomose  with  the  trigeminus  in  their  peripheral  distribution  to  the  scalp  and  chin. 

Special  Anatomy. — A  knowledge  of  the  anatomy  and  physiology  of  the  neck 
muscles  and  nerves  is  important  in  studying  the  more  serious  neuroses  of  this  region. 

Muscles  Function  Nerve  Supply 

_,        ,  j^  .  ,        f  Wrinkles  the  neck,  depresses  the  jaw  and  1  „     .  , 

The  platysma  myoid.. .  S         ,      ,  ,,  ,,  >  Facial. 

[  angle  of  the  mouth.  j 

Recti  capitis  antici.  .  .  .      Flexion  of  head.  C^  and  C^. 

Recti  capitis  laterales .  .      Lateral  movement  and  slight  rotation.       Antr.  branches,  C',^,^.? 

Scaleni  med.  and  post..      Lateral  movement  and  slight  extension.     Antr.  branches,  C^, ? 

„,  ,    .,  J  Lateral    movement;    also     flexion    and  1  „    .      ,  ,  ^„ 

oterno-mastoid -,        ^    , .  .    ,        ,    ^  . ,         .  ,       >  Spmal  accessory  and  C^ 

[  rotation  of   head   to  opposite   side,  j 

Spinal    accessory    and  anterior 


Trapezius {  Lateral  movement  and  extension.      ,    ,  ,  ,  _,        ,   _,, 

[  I    branches  of  C'  and  C*. 

T        ^  ,.  ,.     f  Lateral  movement  and  rotation  to  same  1    .     ,     .       ,  ,         --,„        ,   „, 

Levator  anguli  soapuli.  <      .  ,  >  Anterior  branches,  C^  and  C*. 

I     side.  j 

o  ,     .  ■j_.  /  x^  1       ,  ,      ,  1  1  Ext.    div.    of    post.,    branches    of 

Splemus  capitis <  Draws  head  backward.  }  5,       ' 

1  (     cerv.  nerves.  C^,  C'. 

™       ,    ,  ...  J  Draws    head    backward,    turns    face   to  1  _     ,     ,  ,  „, 

irachelomastoid <  .  ,  „  }  Post,  branches  cerv.  nerve,  C^. 

(    same  side;  J 

/-.,,  f„  11,,  ..,  -il  Post,    branches     cerv.    nerve    C, 

Oomplexus <  Draws  head  back  or  rotates  to  same  side.  >     _,      _ 

^1,.  .  j    Extends  and  slightly  rotates  to  opposite  1  _     ,  ,  i  ^, 

Obhquus  supenos <,       ■■,  ,  ,        ,    ^  •  i  }  Post  branches  cerv.  nerve  C. 

[^    side  and  bends  to  same  side.  J 

Obliquus  inferior Rotates  to  same  side.  Post,  branches  cerv.  nerve,  C^. 

Rectus  cap.  post Extends  and  rotates  to  same  side.  Post,  branches  cerv.  nerve.  Ci. 

The  movements  oi  flexion  of  the  head  are  thus  seen  to  be  due  to  the  sterno-mastoid 
and  anterior  recti  capitis,  innervated  by  the  spinal  accessory  and  by  the  C^  and  C^ 
anterior  branches).  In  forced  flexion  the  hyoid  muscles  come  into  play,  innervated 
by  the  branches  from  the  descendens  and  communicans  hypoglossi,  C^,  C*,  anterior 
branches. 

The  movements  of  extension  are  caused  by  the  complexus,  trachelo-mastoid 
splenius,  obliquus  inferior  and  recti  capitis  postici  and  somewhat  by  the  trapezius. 
These  are  innervated  practically  entirely  by  the  posterior  branches  of  the  cervical 
nerves — from  C^  to  C. 

The  lateral  movements  of  the  head  are  caused  by  the  sterno-mastoid,  splenius, 
scaleni,  trapezius,  complexus,  obliquus  superior,  rectus  capitis  lateralis,  supplied 
by  the  spinal  accessory,  posterior  branches  of  the  cervicals  C^  to  C^,  except  the  recti 
laterales,  supplied  by  the  anterior  branches  C^ 

Extension  and  lateral  movements  of  the  head  are  mainly  done  by  the  spinal  ac- 
cessory and  upper  three  cervical  posterior  branches.  The  sterno-mastoid  gets  some 
branches  from  the  anterior  cervical  division  C^,  as  do  the  recti  capitis  laterales. 


128 


DISEASES    OF   THE    NEEVOUS    SYSTEM 


Eolation  of  the  head  is  caused  by  the  sterno-mastoid,  splenius  trachleo-mastoid, 
complexus,  obliquus  superior  and  inferior,  recti  capitis  postici  and  levator  anguli 
scapuli.  These  are  supphed  by  the  spinal  accessory  and  posterior  branches  of  the 
cervicals  C^  to  C^,  except  the  sterno-mastoid  and  recti  capitis  laterales,  which  is 
supplied  by  the  C^  and  C^  anterior  branches. 

Hence,  after  divsion  of  the  posterior  branches  of  the  cervical  nerves  C^  to  C* 
there  still  remain  innervations  of  the  recti  capitis  laterales  and  levator  anguli  scapuli, 
sterno-mastoid  and  trapezius.  When  the  spinal  accessory  is  cut  these  other  in- 
nervations remain  and  the  head  may  yet  be  extended,  bent  laterally  and  rotated. 

The  muscles  which  rotate  the  head  to  the  same  side  are  the  recti  capitis  lateralis 
(slightly),  levator  anglui  scapuli,  trachleo-mastoid  (posterior  C^),  complexus  (pos- 
terior CS  C^,  C^)  obliquas  inferior  (posterior  C^).     See  diagram,  Fig.  56. 


Antf-Brauck 


Rectus  poslmaj. 

jliq-sup-ifint 
Coiiipl.e>ai; 


Otlic 


•ifm- 
, us 

Sensory  branch  to 
_  ::occinu£ 

CoTTiplexus 

Splentus 

TracheloMast 

Occipital  major] 

Cervical  ascend' 
Trans- colli 
Complexus 

Complexus 
MultifidSpin. 

Iriterspinales 

Semispinales 
Do- 


Fig. 


Do- 

56.- 


■Rectus  lateralis  C'C^ 
Recti  atiteriorC'C^ 

SJD  iapkrag'?^(Phren.)CV 

Slerno  mastoid  C* 
Levator  anq-scap  C^ 
Trapezius  C^C* 

-^  fTrans-ceryical  C^C^ 
■  z\  Aiiri'ci/la  ris  Tna^^C^C 


^  I*-*  '^Supraclavicul-SrcCTJ" 


Diagrammatic  representation  of  the  anterior 
of  the  cervical  nerves. 


and  posterior  divisions 


Those  rotating  to  opposite  side  are  the  sterno-mastoid,  obliquus  superior  (posterior 


Ci). 


The  diseases  of  the  upper  cervical  group  are  spasms,  paralyses  and  neuralgias. 


Spasmodic  Diseases. — ^Torticollis  may  be  limited  to  and  is  usually 
associated  with  the  cervical  nerves,  as  has  been  shown,  though  it  is 
usually  primarily  a  spinal  accessory  neurosis. 

Tonic  spas?n  causing  a  rigid  neck  is  a  frequent  symptom  of  meningitis, 
and  forms  part  of  epileptic  and  other  convulsions. 

In  oscillatory  and  rotatory  spasms  of  the  head  the  cervical  nerves  are 
involved. 


NEUROSES    OF    THE    MOTOR    SPINAL    NERVES  129 

Nodding  Spasm,  Oscillating  Spasm. — ^This  is  a  disorder  occurring 
chiefly  in  children  and  characterized  by  rhythmical  nodding  or  oscillating 
movements  of  the  head.     It  occurs,  however,  in  adults. 

Etiology. — The  disease  occurs  in  young  children  who  are  ansemic 
and  badly  nourished.  Dentition,  digestive  disorders,  eye  defects,  are 
causes.  Sometimes  it  is  only  a  kind  of  habit  spasm,  and  occasionally 
this  habit  continues  during  life.  It  may  be  associated  with  or  be  a  pre- 
cursor of  torticollis.  It  occurs  in  hysteria,  and  sometimes  in  elderly 
people  forming  part  of  a  family  or  senile  tremor. 

Symptoms. — The  condition  in  young  children  is  usually  a  constant 
slow,  mild,  rhythmical,  oscillating  spasm.  It  is  usually  "outgrown." 
In  adults  it  may  assume  the  chronicity  of  a  torticollis  or  it  may  be  plainly 
part  of  a  general  senile  or  family  tremor. 

The  diagnosis  is  easily  made  by  the  symptoms.  The  prognosis  and 
treatment  depend  upon  the  etiology.  I  have  found  bromide  of  potas- 
sium and  hyoscine  useful  in  elderly  cases,  and  syrup  of  iodide  of  iron  in 
children. 

The  phrenic  nerve  arises  from  the  third,  fourth  and  fifth  cervical, 
oftenest  from  the  fourth  and  fifth  (37  per  cent.).  Next  from  the  fourth 
alone  (25  per  cent.)  and  then  from  the  third,  fourth  and  fifth  (23  per 
cent.)  and  from  the  third  and  fourth  (15  per  cent.)  (Schroeder-Green). 

The  diaphragm  is  supplied  by  a  few  filaments  of  the  intercostal  nerves, 
but  these  cannot  take  the  place  of  the  phrenic  and  their  function  is  slight 
(Cavalie). 

In  some  forms  of  stuttering  the  phrenic  nerve  is  involved  in  a  clonic 
or  tonic  spasm. 

Hiccough  is  a  clonic  spasmodic  disorder  of  the  phrenic  nerve.  It 
is  usually  due  in  its  casual  form  to  gastric  disturbance,  with  flatulent 
distention  of  the  stomach. 

When  more  chronic,  it  is  caused  by  hysteria,  neuritis,  diaphragmatic 
pleurisy,  or  some  pressure  upon  the  nerve  in  its  course.  It  is  sometimes 
a  prselethal  symptom.  I  have  seen  cases  in  which  it  was  probably  a  pure 
spasmodic  neurosis,  a  form  of  tic. 

Ordinarily,  hiccough  can  be  stopped  by  simple  carminatives  like 
spirits  of  chloroform  or  lavender  or  a  hot  milk  punch.  In  obstinate 
cases  in  which  no  known  cause  can  be  found,  pilocarpin,  hyoscine  and 
bromides  are  useful.  A  most  effective  measure  is  to  lay  the  patient 
supine  over  a  thick  bolster  so  that  the  head  hangs  back  and  the  thorax 
arches  up.  An  injection  of  morphine  and  atropine  promptly  stops  some 
cases. 

Paralysis  and  Atrophy. — The  cervical  muscles  are  paralyzed  in 
anterior  poliomyelitis,  progressive  muscular  atrophy,  in  jjachymeningitis 

9 


130  DISEASES    OF    THE    NERVOUS    SYSTEM 

hypertrophica,  and  occasionally  in  vertebral  and  peripheral  disease  or 
injury  and  in  spinal-cord  tumors.  Some  deformities  and  weakness  in 
head  movements  result,  but  the  most  serious  consequence  is  involvement 
of  respiration  through  palsy  of  the  phrenic. 

Paralysis  of  the  Phrenic  Nerve — Etiology. — Such  paralysis  may 
be  due  to  disease  or  injury  of  the  cervical  cord  and  also  to  peripheral 
disease,  to  which  the  nerve  is  somewhat  liable  owing  to  its  long  course 
through  the  anterior  mediastinum. 

Pleurisy,  peritonitis,  mediastinal  tumors,  and  multiple  neuritis 
are  among  the  special  causes  of  phrenic  paralysis.  Spinal-cord  dis- 
eases such  as  tabes,  acute  ascending  paralysis,  and  surgical  injuries 
are,  however,  the  commonest  etiological  factors. 

Symptoms. — In  diaphragmatic  paralysis,  if  bilateral,  as  is  usually 
the  case,  the  epigastrium  and  hypochondrium  are  drawn  in  in  inspira- 
tion instead  of  rising.  On  slight  exertion  there  are  dyspnoea  and  in- 
crease of  respiration.     The  cough  is  very  weak. 

Diagnosis.- — If  no  other  muscles  than  the  diaphragm  are  involved, 
the  cause  is  probably  in  the  trunk  of  the  nerve.  Inflammatory  disease 
of  the  diaphragm  may  cause  a  paralysis  which  is  recognized  by  its 
painful  character  and  the  febrile  reaction. 

Treatment. — This  is  to  be  guided  by  the  cause.  It  need  only  be 
said  that  there  is  a  motor  point  in  the  neck  where  by  careful  electriza- 
tion one  can  get  a  contraction  of  the  diaphragm.  In  paralysis  of  the 
phrenic  this  fact  should  be  borne  in  mind. 

GROUP  II.     THE  LOWER  CERVICAL  NERVES  AND  BRACHIAL  PLEXUS 

Anatomy  and  Physiology .^ — The  anterior  branches  of  the  lower  four 
cervical  nerves  and  first  dorsal  nerve  unite  to  form  the  brachial  plexus. 
This  gives  off  short  nerves  to  the  shoulder  and  trunk  and  long  nerves  to 
the  arm. 

The  mode  of  formation  of  the  brachial  plexus  is  shown  in  the  dia- 
gram (Fig.  57).  It  is  in  accordance  with  the  description  by  Cunning- 
ham. The  short  or  upper  branches  supply  the  shoulder  and  intercostal 
muscles.  The  long  or  lower  branches  supply  the  arm  and  hand.  The 
neurologist  needs  to  know:  (1)  the  muscular  distribution  of  each  nerve 
and  the  function  of  the  muscle;  (2)  the  cutaneous  sensory  distribution; 
and  (3)  the  level  of  origin  of  the  nerves. 

The  Plate  II,  Jakob,  Fig.  57,  and  the  table,  p.  132,  give  these  points, 
and  will  be  found  useful  for  study  and  reference.  They  are  based  upon 
the  investigations  of  Ferrier  and  Yeo,  Thorburn,  and  also  on  Abbe's  and 
my  own  experiments. 


NEUROSES    OF    THE    MOTOR    SPINAL    NERVES 


131 


The  Arrangement  of  the  Brachial  Plexus. — ^It  is  made  up  of  three 
nerve  trunks  which  in  turn  make  up  three  cords,  these  cords  giving 
off  various  branches,  thus: 


1.  Trunk    from    sixth    and 
seventh  cervical  roots 


2.  Trunk  from  eighth  cervi-  j 
cal  and  first  dorsal  roots  \ 


3.  Trunk  from  fifth,  sixth, 
seventh,  and  eighth  cer-  ^ 
vical  and  first  dorsal        I 


forms  outer  cord,  which 
gives  off 


forms  inner  cord,  which 
gives  off 


Ext.  ant.  thoracic. 
Musculo-cutaneous. 
Outer  head  median. 
Inner  head  median. 
Llnar. 
Int.  cutan. 
Int.  ant.  thorac. 
Intercost.-hum. 


J.  _,     .  ,    I  Subscapular, 

forms     posterior     cord,  „.  „ 

,  .  ,      .  ™  i  Circumnex. 

which  gives  ott  , ,         ,        .     , 

I  Musculo-spiral. 


N.THORACALIS  ANrERIOR  LATfRALIS 

n-CUTANEOOS 


Fig.  57. — -The  brachial  plexus.     (Cunningham.) 


The  following  table  shows  the  origin,  muscular  distribution,  and 
effect  of  paralysis  on  the  motor  but  not  on  the  sensory  nerves.  This 
latter  is  indicated  in  Figs.  27  and  28. 


132 


DISEASES    OF    THE    NERVOUS    SYSTEM 


Nerves  and  Roots  of  Origin  ,     Muscular  Distribution 


Posterior  thoracic. 
Fifth  and  sixth  cervical. 


Circumflex. 

Fifth  and  sixth  cervical. 

Suprascapular. 


Subscapular,  short. 

Fifth  and  sixth  cervical. 

Subscapular,  long. 

Fifth,     sixth,     seventh     and 

eighth  cervical. 
Anterior  thoracic. 

Musculo-outaneous. 
Fourth  and  fifth  cervical. 
Musculo-spiral. 
Fourth,   fifth,   sixth,   seventh 
and  eighth  cervical. 


Median. 
Fifth,     sixth,     seventh,     and 
eighth  cervical. 


Ulnar. 

Eighth  cervical,  first  dorsal. 


Serratus  magnus. 


Deltoid. 
Teres  minor. 
Supraspinatus. 

and 

Infraspinatus     and     teres 

minor. 
Subscapulares. 
Teres  major. 
Latiss.  dorsi. 


Pectoralis  major. 

Biceps       and      brachialis 

anticus. 
Triceps. 
Supinatores. 

Extensor  carp.  rad. 
Extensor  carp.  uln. 

Extensor  comm.  digit. 

Extensor  p.  i.  pollic. 
Extensor  s.  i.  pollic. 
Extensor  oss.  met.  pollic. 
Pronatores. 
Flexor  carp.  rad. 
Flexor  subUm.  dig. 
Flexor  profund.  dig.  radial 

half. 
Two  lumbricales. 
Abductor  pollic. 
Flexor  pollic. 
Flexor  carp,  ulnar. 

Flexor  profund.  dig.  ulnar 
half. 

Interossei. 
Two  lumbricales. 
Flexor  minor  digit. 
Adductor  pollicis. 
Inner  half  of  flexor  brev. 
pollicis. 


Function  as  Shown  by  Effect  of  Paralysis 


Posterior  edge  of  scapula  is  rotated  out 
when  arm  is  raised  and  carried  forward. 

Weakening  of  elevation  of  shoulder  and  of 
inspiration. 

Loss  of  power  to  raise  arm. 

Weakened    power    to    raise    arm;    head    of 

humerus  tends  to  fall. 
Loss     of     abductors;     motion    forward,   and 

inward  rotation  of  humerus. 
Loss  of  rotation  of  humerus  outward. 

Weakens  inward  rotation  of  arm. 
Weakens  power  of  elevating  shoulder. 
Weakens  power  to  depress  shoulder  and  to 
pull  arm  backward  and  to  side. 

Loss  of  power  to  pull  arm  down  and  forward 

and  to  shrug  the  shoulder. 
Loss  of  flexion  of  forearm. 

Loss  of  extension  of  forearm. 
Loss  of  supination. 

Extension  of  wrist  lost  except  when  fingers 
are  flexed;  lateral  deviation. 

Impaired   extension    of   first   phalanges    and 

wrist. 
Impairment  of  extension  of  thumb. 


Loss  of  pronation. 
Weakened  flexion  of  wrist. 
Weakened  flexion  of  second  and  third  phalan- 
ges of  first  and  second  fingers. 


Loss  of  abduction  and  flexion  of  thumb. 

Weakened  flexion  of  wrist;  radial  deviation. 

Weakened  flexion  of  second  and  third  phalan- 
ges of  third  and  fourth  flngers. 

Loss  of  flexion  of  first  phalanges  and  of  exten- 
sion of  second  and  third. 


Diseases  of  the  Lower  Cervical  Nerve  Group  and  the  Brachial 
Plexus.- — ^The  nerves  of  this  group  are  subject  to  the  pathological  dis- 
turbances common  to  all  nerves.  I  shall  describe  them  from  the  clinical 
side,  which  gives  the  following  disorders: 


NEUROSES    OF    THE    MOTOR    SPINAL    NERVES  133 

f  Combined  arm  palsies. 
Upper-arm  type  or  Erb's  paral3'sis. 


Paralyses ,  t  ^  -r^,         ,    ,  ,     . 

I  Lower-arm  type.     Ivlumpke  s  paralysis. 

[  Paralyses  of  individual  nerves. 
Spasmodic  Disorders \  Occupation  neuroses 

f  Brachial  neuralgia. 
Sensory  Disorders \  Digital  neuralgia. 

JNumb  hands  (acroparsesthesia). 
Neurotic  oedema. 
Symmetrical  gangrene. 

Spasmodic  Disorders  of  the  Arm. — The  arms  and  hands  are  es- 
pecially subject  to  tremors,  choreic  and  other  spasmodic  movements. 
The  only  spasmodic  disorders,  however,  which  may  be  said  to  be  es- 
pecially located  there  are  writer's  cramp  and  allied  occupation  neuroses. 
These  are  described  elsewhere. 

Brachial  Paralyses,  Arm  Palsies. — These  occur  as  combined  or 
total-arm  palsies,  upper-arm  and  lower-arm  types,  and  paralyses  of 
single  nerves. 

Combined  paralysis  of  the  brachial  nerves  is  a  condition  in  which 
all  or  nearly  all  the  portions  of  the  plexus  and  its  branches  are  involved. 
Total-arm  palsies  make  up  about  6  per  cent,  of  all  peripheral  paraly- 
ses, and  are  about  one-fifth  as  frequent  as  single-nerve  paralyses. 

Etiology. — They  occur  oftenest  in  men,  but  are  not  rare  in  infants, 
being  then  due  to  injuries  during  parturition.  After  infancy  they  are 
most  frequent  in  early  and  middle  life. 

The  exciting  causes  are  obstetrical  injuries;  wounds,  cuts,  fractures; 
deep-seated  inflammations  and  tumors;  shoulder  dislocations;  primary 
neuritis;  crutch  and  other  forms  of  mechanical  compression;  hysteria; 
in  rare  cases,  spinal-cord  and  brain  disease. 

The  symptoms  vary  with  the  severity  and  extent  of  the  lesion. 

With  regard  to  severity,  there  are  three  degrees.  In  the  first  there  is 
simply  a  transient  palsy,  due  to  lying  too  long  on  the  arm.  The  arm 
feels  heavy,  numb  and  /'asleep."  In  a  few  minutes  or  hours  this  palsy 
disappears.  In  the  second  degree  the  nerves  are  so  much  compressed 
as  to  be  mechanically  injured.  If  the  patient  has  been  drinking  hard, 
even  moderate  pressure  may  set  up  an  inflammatory  or  destructive 
process  that  leads  to  quite  a  serious  palsy.  In  the  third  degree  the  nerves 
are  actually  cut  or  torn  across,  or  so  compressed  as  to  lose  their  anatomical 
integrity. 

The  resulting  symptoms  are  those  common  to  all  nerve  injuries,  viz., 
paralysis,  wasting,  changes  in  electrical  reaction  of  the  muscles.  Pain, 
tenderness,  anaesthesia,  trophic,  secretory  and  vasomotor  disturbances 
are  also  present  in  varying  degree. 


134 


DISEASES    OF   THE    NEKVOUS    SYSTEM 


The  distribution  of  the  paralysis,  atrophy,  and  sensory  disturbance 
depends,  of  course,  upon  the  arm  nerves  chiefly  involved.  The  cuts 
and  table  will  enable  one  to  see  in  any  case  where  the  trouble  is  localized. 

It  is  important  to  determine  whether  one  is  dealing  with  a  total- 
arm  palsy,  an  upper-arm  type  (Erb's  palsy),  or  a  lower-arm  type. 

In  Erb's  palsy  there  is  involvement  of  the  deltoid,  biceps,  brachialis 
anticus  and  supinator  longus,  with  at  times  paralysis  of  the  supinator 
brevis,  infraspinatus  and  even  of  all  the  muscles  supplied  by  the  median 
nerve.     The  lesion  is  either  in  the  cord  formed  by  the  fifth  and  sixth 


Fig.  58. — Upper-arm  palsy  of  left  side. 

cervical  nerves  or  a  little  lower  in  the  brachial  plexus,  where  the  fibres 
supplying  the  musculo-spiral,  circumflex  and  musculo-cutaneous  lie 
close  together.  At  all  events,  the  lesion  involves  the  central  parts  and 
upper  cords  of  the  plexus.  The  arm  hangs  by  the  side  and  the  forearm 
cannot  be  flexed  (Fig.  58).  There  are  many  variants  of  the  upper-arm- 
shoulder  paralysis  due  to  surgical  injuries,  tumors,  passive  hanging  by  the 
hands  by  gymnasts,  etc. 

The  upper-arm  type  is  especially  frequent  in  infants  and  constitutes 
one  of  the  obstetrical  paralyses.  The  trouble  is  caused  through  com- 
pression and  tearing  of  the  upper  cords  of  the  plexus  in  difficult  labor. 
Among  thirty  cases  collected  by  Dr.  A.  S.  Leverty,  twenty-eight  were 


NEUROSES    OF   THE    MOTOR   SPINAL   NERVES 


135 


difficult  head  presentations.  Sometimes  there  is  a  hemorrhage  in  the 
cord  itself. 

In  the  lower-arm  type  (Klumpke's  paralysis)  the  triceps,  the  flexors  of 
the  wrist,  the  pronators,  the  flexors  and  extensors  of  the  fingers  and  the 
hand  muscles  are  involved.  The  arm  can  be  raised  and  the  forearm 
flexed  and  supinated,  but  the  hand  is  useless  and  the  extension  of  the 
forearm  is  impossible.  The  lesion  here  involves  chiefly  the  nerves  from 
the  seventh  and  eighth  cervical  and  first  dorsal  roots  (Fig.  59). 

If  the  lesion  is  in  the  nerve  there  will  be  atrophy,  changes  in  electrical 
reaction,  sensory  disturbances,  and  often,  if  there  is  neuritis,  pain  over 
the  nerves.  The  reflexes  will  be  lessened  or  absent.  If  the  lesion  is  in 
the  spinal  cord,  symptoms  in  other  parts  of  the  body  will  be  present,  or, 


Fig.  59. — Lower-arm  palsy  and  wrist-drop. 


if  not,  there  will  be  no  sensory  disturbance,  as  in  an  arm  palsy  from 
anterior  poliomyelitis.  In  rare  cases  arm  palsies  may  be  caused  by 
spinal  tumors  or  a  local  meningitis,  in  which  case  the  oculo-pupillary 
centre  of  the  cervical  cord  and  the  sympathetic  may  be  involved. 

There  are  three  common  symptoms,  however,  of  which  it  is  often 
very  important  to  analyze  the  cause.  These  are  the  loss  of  power  for 
elevation  of  the  arm  and  for  flexion  and  extension  of  the  forearm. 

Flexion  of  the  forearm  is  performed  by  the  biceps  and  brachialis  anticus, 
and  is  helped  by  the  supinator  longus.  These  muscles  are  supplied  by 
the  musculo-cutaneous  nerve,  except  the  supinator,  which  is  supplied  by 
the  musculo-spiral.  Hence  when  a  person  cannot  flex  the  forearm,  the 
musculo-cutaneous  is  chiefly  affected. 


136 


DISEASES    OF    THE    NERVOUS    SYSTEM 


Extension  of  the  arm  is  done  by  the  triceps,  which  is  supphed  by  the 
musculo-spiral. 

Elevation  of  the  Arm  Outward.- — InabiHty  to  raise  the  arm  is  the 
common  and  striking  symptom  in  combined  brachial  palsies.  The  arm 
is  raised  by  a  number  of  muscles.  The  deltoid  acts  first  and  most, 
but  it  can  raise  the  arm  only  to  a  right  angle.  It  is  supplied  by  the  cir- 
cumflex nerve  from  the  posterior  cord  of  the  plexus.  After  the  arm  is 
raised  to  a  right  angle,  it  is  further  elevated  by  rotating  the  scapula, 
and  this  is  done  chiefly  by  the  middle  part  of  the  trapezius  (lower  cervical 
and  upper  dorsal  nerves)  and  by  the  serratus  magnus,  supplied  by 
the  posterior  thoracic  nerve.  A  number  of  other  muscles  combine  to 
strengthen  elevation  of  the  shoulder,  but  this  action  can  be  abolished 
only  by  paralysis  of  the  deltoid  or  trapezius  and  serratus  magnus. 


Fig.  60. — Illustrating  the  formation  of  the  brachial  plexus;  also  the  involvement  of 
the    plexus    in    degenerative    neuritis.     (Leszynsky.) 


The  diagnosis  of  these  cases  involves,  first,  consideration  of  the  seat 
of  the  lesion  and  the  special  nerves  involved;  next,  that  of  the  nature 
of  the  lesion.  A  recognition  of  the  seat  of  the  lesion  and  of  the  special 
nerves  involved  depends  entirely  upon  the  study  of  the  distribution  of 
the  palsy  and  of  the  atrophy  and  sensory  disturbance. 

The  prognosis  in  arm  palsies  as  a  whole  is  usually  good  except  for 
the  total-arm  palsies.  Nearly  all  these  cases  get  well,  the  duration  of 
the  incapacity  being  from  two  or  three  months  to  a  year.  Even  in  the 
severest  cases  recovery  is  possible  after  one  or  two  years.  If,  however, 
the  nerves  are  torn  across,  as  in  birth  palsies,  and  the  ends  widely  sepa- 
rated, recovery  is  impossible  unless  an  operation  is  promptly  done. 

The  treatment  consists  in  electrical  applications,  educational  move- 
ments, mechanical  support,  with  potassium  iodide  internally  and  absti- 


NEUKOSES    OF    THE    MOTOR    SPINAL    NERVES 


137 


nence  from  alcohol.     Local  injections  of  nitrate  of  strychnine  are  useful, 
and  massage  should  be  used  if  it  can  be  applied  carefully. 

In  brachial  palsies  due  to  severe  injuries,  dislocations,  fractures, 
etc.,  in  which  there  is  evidence,  from  the  extreme  atrophy  and  absence 
of  electrical  reaction,  that  the  nerve  is  entirely  cut  across  and  that  the 
ends  are  not  in  apposition,  a  surgical  operation  is  stringently  needed. 
The  nerves  should  be  exposed  and  the  ends  brought  as  near  together  as 
possible.  When  this  cannot  be  done,  the  nerves  can  be  split  and  the 
ends  sutured  or  anastomoses  made,  or  the  two  ends  are  sewed  together  as 


Fig.  61. — Double    paralysis    of    circumflex    nerve. 


near  as  possible  and  placed  in  a  tube.  If  the  separation  is  over  an  inch, 
not  much  can  be  expected.  In  all  these  cases,  however,  it  must  be 
remembered  that  the  two  ends  do  not  unite,  but  the  central  end  grows 
down  in  the  tract  of  the  old  degenerated  peripheral  stem. 

Paralysis  of  Single  Nerves — Paralysis  of  the  Posterior  Thoracic 
Nerve — Etiology.- — This  rare  trouble  usually  occurs  in  male  adults  and 
is  due  to  injury  or  sudden  strains.  Its  paralysis  may  be  part  of  a 
progressive  muscular  atrophy.     The  nerve  goes  to  the  serratus  magnus. 

Symptoms. — When  paralyzed,  there  is  difhculty  in  raising  the  arm 
above  the  horizontal  position  and  the  movements  of  the  shoulder  are 


138  DISEASES    OF    THE    NERVOUS    SYSTEM 

weakened.  When  the  arm  hangs  by  the  side  the  lower  angle  of  the 
scapula  is  drawn  a  little  nearer  the  vertebral  column  and  protrudes  slightly. 
When  the  arm  is  held  out  horizontally  the  inner  edge  of  the  scapula 
protrudes  and  is  drawn  toward  the  middle  line.  When  the  raised  arm 
is  brought  forward  there  is  a  deep  groove  formed  between  the  inner 
border  of  the  scapula  and  the  thoracic  wall  (Fig.  65). 

The  disease  often  runs  a  long  course  and  is  accompanied  by  pain. 

Paralysis  of  the  Circumflex  Nerve. — The  nerve  goes  to  the  deltoid, 
teres  minor,  third  head  of  the  triceps  and  shoulder-joint.  It  gives 
sensation  to  the  skin  of  the  shoulder.  It  is  very  often  paralyzed.  The 
commonest  causes  are  a  fall  or  injury,  dislocation  and  rheumatic  inflam- 
mation of  the  joint.  The  arm  cannot  be  elevated  or  rotated  outward 
(Fig.  61).     There  are  atrophy,  anaesthesia  and  sometimes  pain. 

Paralysis  of  the  Suprascapular  Nerve. — The  nerve  goes  to  the  spinati 
muscles,  teres  minor  and  shoulder-joint.  Disease  of  this  nerve  alone 
is  rare. 

The  supraspinatus  rotates  the  shoulder  in,  the  infraspinatus  and 
teres  minor  rotate  it  out.  When  paralyzed,  there  is  an  impairment  of 
rotation  and  some  impairment  of  elevation  of  the  shoulder. 

Paralysis  of  the  Musculo-spiral  Nerve  {Wrist-drop,  Lead  Palsy, 
Compression  Paralysis). — ^The  distribution  of  this  nerve  is  given  in  the 
table  and  cut.  Its  function  is  to  extend  and  supinate  the  forearm,  to 
extend  the  wrist  and  fingers,  and  slightly  to  adduct  and  abduct  the  fingers. 
It  extends  directly  only  the  last  or  ungual  phalanges,  the  first  and 
second  phalanges  being  extended  by  the  ulnar  nerve. 

Etiology. — The  musculo-spiral,  owing  to  its  course,  is  the  most 
frequently  affected  by  paralysis  of  all  the  arm  nerves.  Pressure  on  the 
nerve  during  sleep — especially  when  the  patient  is  intoxicated,  crutch 
pressure,  fractures,  wounds,  tumors,  lead  poisoning,  arsenical,  alcoholic 
and  other  forms  of  multiple  neuritis  are  the  causes  of  its  disordered 
function. 

Symptoms. — The  symptoms  of  this  paralysis  are  ''wrist-drop,"  due 
to  an  inability  to  extend  the  wrist  or  fingers.  The  first  and  second 
phalanges  can  be  extended  somewhat  by  the  interossei  and  lumbricales, 
but  the  last  phalanges  cannot  be  extended  at  all.  The  first  finger  is  least 
affected.  The  fingers  can  be  only  slightly  abducted,  supination  is 
generally  lessened  or  lost;  if  the  lesion  is  high  up,  the  triceps  is  involved 
and  the  power  of  extending  the  forearm  weakened.  There  may  be 
atrophy  of  the  muscles  and  degeneration  reaction.  A  swelling  over  the 
tendons  of  the  wrist-joint  may  occur.  Some  numbness  and  tingling 
exist,  and  occasionally  there  is  anaesthesia  in  the  distribution  of  the  radial 
nerve  on  the  hand.     The  disease  lasts  but  a  few  weeks  if  due  to  com- 


NEUROSES    OF   THE    MOTOR   SPINAL   NERVES 


139 


pression;  for  months  if  due  to  neuritis,  lead  poisoning  or  severe  injury 
of  the  nerve.     Eventually  recovery  takes  place,  as  a  rule. 

When  the  disease  is  due  to  lead  poisoning  there  are  some  peculiarities 
in  its  course.  Thus  the  supinator  longus  usually  escapes;  the  palsy 
begins  gradually  and  usually  involves  both  arms;  it  may  extend  to 
the  upper  arm.  Partial  degeneration  reactions  are  present.  There  is 
rarely  any  ansesthesia  and  but  little  pain.  Often  there  is  a  lead  line  on 
the  gum  and  a  history  of  constipation  and  colic. 

In  alcoholic  and  other  forms  of  multiple  neuritis  there  are  pain  and 
parsesthesia,  both  arms  are  involved,  and  the  flexors  and  other  fore- 


FiG.  62. — 'Wrist-drop  from  lead  palsy. 


Fig.  63.— (a)  Paralysis  of  radialis  and 
median  nerves  with  anasthesia  (b)  paraly- 
sis of  radialis.     {Leverty.) 


arm  muscles  are  somewhat  implicated.  There  are  marked  sensory 
disturbances.     The  legs  are  also  affected. 

In  compression  palsy  the  supinators  and  often  the  triceps  are  involved. 

When  the  lesion  of  the  nerve  is  high  up,  as  in  crutch  paralysis,  there 
is  but  little  ansesthesia,  and  that  is  found  on  the  anterior  surface  of 
the  forearm,  in  the  distribution  of  the  external  and  internal  cutaneous 
nerves.  Lesion  of  the  nerve  lower  down  may  give  rise  to  some  ansesthesia 
along  the  radial  border  of  the  forearm  and  back  of  hand,  but  the  anses- 
thetic  area  varies  a  great  deal. 

The  diagnosis  of  the  paralysis  is  easily  made.  The  most  important 
point  is  to  find  out  the  cause.  The  different  characteristics  of  lead 
palsy,  neuritic  palsy  and  compression  palsy  have  been  indicated  in  the 


140  DISEASES    OF    THE    NEEVOUS    SYSTEM 

description  of  the  symptoms.  One  must  be  sure  to  exclude  also  pro- 
gressive muscular  atrophy. 

The  treatment  consists  of  mechanical  measures,  such  as  electricity, 
massage,  the  application  of  rubber  muscles  and  in  bad  cases  the  fixation 
of  the  forearm  and  hand  in  hyperextension  by  means  of  a  splint  and 
plaster-of -Paris  bandage  (Gibney).  Internally  in  the  early  stage  it  is 
best  to  administer  iodide  of  potassium  and  sulphate  of  magnesium  (in 
lead  palsy),  the  salicylates  in  neuritis;  later,  hypodermic  injections  of 
strychnine  may  be  given.  Static  sparks,  galvanism  and  other  forms  of 
electricity  unquestionably  do  good  in  some  cases. 

Paralysis  of  the  median  nerve  is  rare  as  an  isolated  trouble,  and  is 
almost  always  due  to  injury  or  neighboring  disease. 

When  paralysis  occurs  the  grip  is  weakened.  Flexion  and  abduction 
of  the  thumb  and  flexion  of  the  first  and  second  fingers  are  impaired. 
Atrophy  of  the  thenar  eminence  may  occur.  The  anaesthetic  area  varies, 
but  is  shown  in  the  accompanying  cut  (Fig.  63). 

Paralysis  of  the  Ulnar  Nerve — Etiology. — The  ulnar  nerve  is  rather 
commonly  affected  by  paralysis,  the  occurrence  ranking  next  in  fre- 


FiG.  64. — Paralysis  of  ulnar. 

quency  to  musculo-spiral  palsy.  It  is  rarely  affected  in  lead  poisoning, 
but  is  usually  early  involved  in  progressive  muscular  atrophy.  It  is 
sometimes  attacked  by  a  primary  degenerative  neuritis.  Injuries  are 
the  common  cause. 

The  symptoms  are  shown  by  the  table  (p.  130).  The  hand  cannot 
be  closed  tightly,  the  little  and  ring  fingers  being  especially  weak.  The 
first  phalanges  are  drawn  back  and  the  second  and  third  phalanges 
flexed;  when  the  interossei  and  lumbricales  atrophy,  the  result  is  the 
"griffin  claw"  or  main  en  griff e.  The  fingers  cannot  be  adducted  or 
abducted  except  feebly. 

There  is  anaesthesia  over  the  area  of  distribution  of  the  ulnar  (Fig. 
64) ;  there  may  be  pain  and  tenderness. 


NEUEOSES    OF    THE    MOTOR    SPINAL    NERVES 


141 


Migrating  neuritis  is  a  serious  but  rare  malady  which  deserves  some 
mention.  It  occurs  as  a  sequel  to  some  wound  of  or  operation  upon  a 
nerve.  The  local  neuritis  extends  usually  up  the  arm  (ascending  neuritis) . 
It  is  accompanied  by  intense  pain,  anaesthesia,  paralysis  and  atrophy. 
The  disease  is  very  chronic  and  intractable.  It  has  been  relieved  in 
some  cases  by  resecting  the  posterior  spinal  roots. 

Morvan's  Disease,  Analgesic  Pa- 
ralysis with  Whitlow. — (Neuritic  type 
of  syringo-myelia.) 

This  is  a  very  rare  disease,  char- 
acterized by  a  slowly  progressive  pa- 
ralysis and  atrophy  of  the  hands  and 
forearms,  with  analgesia  and  painless 
whitlows.  It  is  probably  always  ei- 
ther a  form  of  syringo-myelia  or  of 
leprosy. 


GROUP  III. 


THE  THORACIC  OR  DOR- 
SAL NERVES 


Fig.  65. — Paralysis  of  right  poste- 
rior and  thoracic  nerve  and  serratus 
magnus  muscle. 


Anatomy  and  Physiology. — The  dorsal 
nerves  are  twelve  in  number.  The  first  is 
the  largest  and  belongs  functionally  to  the 
arm  nerves.  The  dorsal  nerves  carry  motor 
and  sensory  fibres  to  the  voluntary  muscles, 
skin  and  other  tissues  of  the  trunk  wall. 
They  carry  some  splanchnic  fibres  to  the 
lungs  and  abdominal  viscera.  They  divide 
into  anterior  and  posterior  branches.  The  anterior  form  intercostal  nerves,  of  which 
the  first  six  are  distributed  to  the  wall  of  the  thorax  and  the  last  six  to  the  wall  of  the 
abdomen.  All  these  nerves  give  off  lateral  and  anterior  branches.  The  posterior 
branches  of  the  dorsal  nerves  are  small  and  supply  the  muscles  and  skin  of  the  back. 

The  upper  six  dorsal  nerves,  including  both  branches,  are  mainly  inspiratory 
in  function.  They  also  extend  and  rotate  the  dorsal  and  cervical  vertebrae.  The 
lower  dorsal  are  expiratory  nerves;  they  also  assist  in  compressing  the  abdominal 
viscera  and  in  flexing,  extending  and  rotating  the  spine. 

Motor  Neuroses. — ^The  thoracic  motor  nerves  are  mainly  involved 
in  respiratory  cramps  and  paralyses;  sneezing,  coughing,  laughing 
and  crying  are  symptoms  in  which  they  play  a  large  part.  In  com- 
plete respiratory  paralysis  also  these  nerves  are  affected.  But  there 
are  few  motor  neuroses  that  are  limited  to  the  thoracic  nerves.  The 
neuroses  of  these  parts  are  mainly  sensory  and  will  be  described  later. 

GROUP  IV.     THE  LUMBAR  NERVES 

Anatomy  and  Physiology. — The  lumbar  nerves  are  five  in  number.  The  posterior 
branches  supply  the  erector  spinae,  interossei,  multifidus  spinae  and  interspinales,  and 


142 


DISEASES    OF    THE    NERVOUS    SYSTEM 


also  the  skin  of  the  back.  The  anterior  branches  of  the  upper  four  unite  to  form  the 
lumbar  plexus.  The  fifth  or  lumbo-sacral  nerve  sends  most  of  its  fibres  to  the  sacral 
plexus.  The  branches  of  the  lumbar  plexus  are:  (1)  the  ilio-inguinal,  (2)  ilio- 
hypogastric (from  first  lumbar),  (3)  genito-crural,  and  (4)  external  cutaneous  (mainly 
from  the  second),  (5)  obturator  (from  third  and  fourth  lumbar),  (6)  the  anterior  crural 
(from  second,  third  and  fourth — Plate  II). 

The  first  four  branches  of  the  plexus  are  comparatively  short  and  supply  sensation 


WHITE  RAMUS 

TE  RAMUS 


NERVE  TO  HAMSTRING   MUSCLES 


Fig.  66. — The  lumbar  and  sacral  plexuses.     {Cunningham.) 

to  the  abdominal  wall  and  external  genitals.  The  last  two  are  longer  and  supply  the 
hip-  and  knee-joints,  the  muscles  of  the  anterior  inner  and  outer  part  of  the  thigh,  the 
skin  over  this  region  and  the  inner  side  of  the  leg  and  dorsum  of  the  foot  (Figs.  27  and 
28). 

The  diseases  of  the  lumbar  nerves  and  plexus  so  far  as  they  form  independent 
disorders  are  mainly  neuralgias.  In  making  a  diagnosis  of  lumbar-nerve  disease,  one 
should  remember  that  of  the  six  branches  of  the  plexus  the  upper  four  are  mainly 
sensory,  the  lower  two  mixed  nerves. 


NEUROSES    OF    THE    MOTOR    SPINAL    NERVES  143 

Paralyses  and  spasmodic  troubles  of  the  lumbar  nerves  are  not  rare, 
but  are  usually  symptomatic  of  some  extrinsic  and  often  serious  disease. 

Etiology. — Hence  it  is  well  to  catalogue  here  those  affections  which 
may  produce  lumbar  palsies  or  spasms.  They  are  pelvic  tumors  or 
injuries,  impacted  faeces,  caries  of  the  spine,  psoas  abscess,  obturator 
hernia,  hip  disease  and  pressure  of  the  foetal  head. 

Symptoms. — When  the  upper  two  lumbar  nerves  are  involved, 
only  sensory  symptoms  in  the  distribution  of  their  branches  occur. 
If  the  next  two  are  also  involved,  there  may  be  trouble  in  extending 
the  leg  and  flexing  the  hip  on  the  trunk.  The  patient  cannot  raise  him- 
self to  a  sitting  posture.  If  there  are  irritation  and  spasm,  the  thigh  is 
drawn  up  and  adducted. 

In  paralysis  of  the  obturator  nerve  there  are  loss  of  power  to  adduct 
the  thigh  and  cross  the  leg  and  weakness  of  outward  rotation  of  the 
thigh.     Anaesthesia  over  the  inner  side  of  the  thigh  may  be  present. 

In  paralysis  of  the  anterior  crural  nerve  there  are  weakness  of  the 
muscles  of  the  anterior  region  of  the  thigh,  loss  of  power  of  extend- 
ing the  leg,  and  anaesthesia  or  pain  over  the  crural  area. 

Paralysis  of  the  posterior  branches  of  the  lumbar  nerves  causes  weak- 
ness or  paralysis  of  the  erectors  of  the  spine.  The  lumbar  curve  is 
very  greatly  exaggerated,  the  shoulders  being  thrown  far  back  and 
the  belly  protruding.  This  condition  occurs  in  progressive  muscular 
dystrophy,  particularly  in  the  pseudo-hypertrophic  form. 

GROUP  V.     THE  SACRAL  NERVES 

Anatomy  and  Physiology. — ^Tlie  sacral  nerves  are  five  in  number.  The  first  four 
divide  into  anterior  and  posterior  branches.  The  fifth  has  no  anterior  branch.  The 
posterior  branches  escape  through  the  posterior  sacral  foramina  and  supply  the 
multifidus  spinse  and  the  skin  over  the  sacrum  and  coccyx. 

The  first  three  anterior  branches,  with  the  lumbo-sacral  nerve  and  a  branch  from 
the  fourth  sacral,  unite  to  form  the  sacral  plexus.  This  lies  upon  the  pyriformis  mus- 
cle in  the  pelvis,  and  escapes  at  the  lower  part  of  the  sacro-sciatic  foramen.  The 
great  mass  of  the  fibres  go  to  make  up  the  sciatic  nerve. 

The  roots  of  origin  of  the  sacral  and  coccygeal  nerves  form  the  cauda  equina. 

The  branches  of  the  sacral  plexus  are  the  superior  gluteal,  muscular,  small  sciatic, 
inferior  gluteal,  pudic,  great  sciatic,  perforating,  cutaneous  and  articular.  These 
are  distributed  to  the  muscles,  skin  and  joints  of  the  buttocks,  thighs,  legs  and  feet. 
The  sensory  distribution  is  shown  in  Figs.  27  and  28. 

The  sacral  nerves  are  the  main  agents  in  station  and  locomotion.  They  control 
the  legs  entirely,  also  the  posterior  muscles  of  the  thigh  and  buttocks;  they  give  sensa- 
tion to  these  parts.  They  carry  also  fibres  that  regulate  the  sexual  function,  bladder 
and  rectum.  From  the  sacral  portion  of  the  cord  there  is  an  outflow  of  nerves  to  the 
autonomic  system,  thence  to  the  pelvic  organs. 

The  diseases  of  the  sacral  nerves  may  be  classified  in  a  similar  way  to  those  of  the 
brachial  plexus. 


144  DISEASES    OF    THE    NERVOUS    SYSTEM 

Spasmodic  Disorders  of  the  Sacral  Nerves. — Tremor,  rigidity, 
clonic  and  tonic  spasms,  myoclonus,  athetoid  movements  all  affect 
the  lower  extremities,  but  they  are  almost  invariably  part  of  some 
general  or  central  disorder,  such  as  chorea,  paralysis  agitans,  hysteria, 
etc.  Under  the  head  of  occupation  neuroses  there  occur  certain  rare 
spasmodic  troubles  special  to  the  legs.  Saltatory  spasm  involves  the 
legs  alone.     These  disorders  are,  however,  general  neuroses. 

Peripheral  Leg  Palsies. — Paralyses  of  the  lower  limbs  from  disease 
of  the  nerves  may  be  either  combined  or  single,  just  as  is  the  case  with 
arm  palsies. 

A  combined  sacral  palsy  is  one  in  which  all  or  nearly  all  of  the  branches 
of  the  sacral  plexus  are  involved. 

Etiology. — Such  palsies  are  due  to  much  the  same  causes  as  those 
affecting  the  lumbar  nerves,  viz.,  injury,  dislocation,  hip  disease,  tumors 
and  neuritis.     Hysteria  may  cause  a  functional  sacral  palsy. 

Symptoms. — The  symptoms  are  indicated  by  a  study  of  the  dis- 
tribution of  the  nerves,  varying,  however,  in  degree.  The  foot  cannot 
be  moved;  the  leg  can  be  slightly  extended  by  the  anterior  crural,  but  not 
flexed;  the  thigh  cannot  be  extended  freely  or  rotated  perfectly. 
There  is  anaesthesia  over  the  distribution  of  the  sacral  nerves;  pain  may 
be  present;  wasting  and  vasomotor  and  secretory  disturbances  occur 
unless  the  paralysis  is  functional. 

The  course  depends  on  the  severity  of  the  lesion.  If  the  nerve  is 
totally  cut  or  torn  across,  it  may  require  one  or  two  years  for  perfect 
recovery  which,  however,  occurs  if  the  severed  ends  are  properly 
approximated. 

The  diagnosis  of  a  sacral  palsy  is  based  on  the  history  and  on  the 
distribution  of  the  anaesthesia  and  of  the  muscular  paralysis.  The 
sacral  nerves  do  everything  for  the  lower  limb  except  extend  the  leg, 
flex  and  adduct  the  thigh,  and  to  some  extent  rotate  it.  They  supply 
sensation  equally  extensively. 

The  distinction  from  spinal-cord  disease  is  chiefly  based  on  the 
unilateral  symptoms,  the  absence  of  disorder  of  the  sphincters  and  the 
combination  of  paralysis,  wasting  and  sensory  troubles  in  the  course  of 
the  sacral  nerves. 

Single-nerve  Sacral  Palsies.— The  symptoms  of  paralysis  of  single 
nerves  are  indicated  by  their  function.  The  nerves  rarely  affected  are 
the  superior  gluteal,  muscular  and  small  sciatic.  The  nerve  oftenest 
affected  is  the  great  sciatic,  and  especially  its  anterior  tibial  branch.  In 
the  latter  case  a  condition  called  ''drop-foot"  is  produced. 

In  the  pathology  and  treatment  of  sacral  palsies  there  is  nothing  especial 
that  can  be  said. 


CHAPTER  X 
SENSORY  NEUROSES  OF  THE  CEREBROSPINAL  NERVES 

As  the  most  common  disorders  of  the  sensory  nerves  are  neuralgias 
and  paresthesias,  I  shall  introduce  the  subject  with  a  general  description 
of  these  symptoms. 

PARESTHESIA 

LOCAL    PARESTHESIA  ACRO-PARESTHESIA,  WAKING   NUMBNESS 

The  condition  known  as  paresthesia  is  one  which  should  be  more 
familiar  to  physicians  and  be  more  commonly  recognized  and  under- 
stood. Parcesihesia  is  the  name  given  to  a  number  of  subjective  sen- 
sations, such  as  prickling,  numbness,  creeping  sensations,  tickling  and 
burning.  It  includes,  in  fact,  nearly  all  the  subjective  sensations  of  the 
skin,  except  those  of  pain.  It  is  a  condition  which  is,  therefore,  extremely 
common,  and  in  its  mildest  and  most  trivial  character  is  much  more  often 
experienced  than  pain.  When  these  sensations  fix  themselves  in  a  certain 
locality,  following  perhaps  the  tract  of  the  nerve  or  fastening  themselves 
upon  the  hand  or  foot,  they  take  on  a  certain  clinical  type,  and  deserve 
to  have  the  name  of  a  disease  to  just  the  same  extent  that  a  neuralgia 
does.  Paresthesia,  in  almost  all  cases,  implies  simply  a  lower  grade 
of  irritation  of  the  nerve-fibres  that  occurs  in  neuralgia,  and  is  a  kind  of 
ghostly  simulacrum  of  that  disease.  It  very  often  precedes  or  accom- 
panies attacks  of  pain.  There  is  sometimes  a  tingling  of  the  teeth  or 
burning  in  the  face  which  has  a  shadowy  likeness  to  a  toothache  or  tri- 
geminal neuralgia.  In  the  same  way,  one  finds  paresthesias  affecting 
the  head,  causing  sensations  of  pressure  and  constriction,  of  burning, 
and  general  undefinable  discomfort,  which  are  entirely  comparable  to 
headaches. 

In  conditions  of  neurasthenia,  paresthesias  of  the  head  are  more 
common  even  than  the  headaches.  Paresthesia  sometimes  follows  the 
course  of  a  nerve,  as  when  one  feels  numbness  of  the  hand  if  the  ulnar 
is  pressed  upon  at  the  elbow,  or  numbness  in  the  foot  where  the  sciatic  is 
pressed  upon,  as  when  the  legs  are  crossed. 

There  is  also  paresthesia  affecting  one  of  the  intercostal  nerves  or 
one  of  the  crural  nerves.  On  the  other  hand,  paresthesia  may  affect 
all  four  extremities,  so  that  they  feel  entirely  benumbed  or  prickling. 

145 

10 


146  DISEASES    OF    THE    NERVOUS    SYSTEM 

Parsesthesia  is  usually  peripheral  and  neuritic,  but  it  may  be  cerebral 
and  due  to  cord  or  brain  disease. 

Etiology. — Parsesthesia,  whether  local  or  diffuse,  occurs  rather  more 
often  in  women  than  in  men,  and  rather  more  often  in  the  mature  and 
middle-aged  than  in  young  people.  It  is  most  frequent  in  women  of 
middle  age,  especially  in  those  who  are  accustomed  to  hard  work  with 
the  hands  in  washing  and  the  exposure  incidental  to  this.  It  also  occurs 
in  those  who  are  obliged  to  walk  a  great  deal  and  to  be  upon  their  feet,  and 
it  especially  affects  tailors,  seamstresses,  bookbinders  and  those  who  have 
to  use,  their  hands  constantly  in  some  skilled  mechanical  work.  It 
sometimes  occurs  in  old  age,  being  accompanied  by  evidence  of  gout  or 
by  glycosuria.  It  is  associated  with  rheumatism  and  with  alcoholism. 
It  follows  infections  like  typhoid  fever  and  the  grippe,  and  means  in 
these,  as  in  many  other  cases,  a  low  grade  of  neuritis. 

Parsesthesias  which  at  first  are  due  to  some  direct  or  reflex  nerve 
irritation  may  become  a  habit  and  form  a  part  of  a  psychosis.  Par- 
aesthesias  are  very  common  in  melancholia  and  hypochondria. 

Cerebral  paraesthesias  occur  in  tabes,  combined  sclerosis  and  in 
thalamic    lesions. 

Parsesthesia  affects  single  cerebrospinal  nerves  just  as  neuralgia 
does,  or  it  may  be  more  generally  distributed.  In  the  latter  case  it 
affects  often  the  feet  and  hands,  and  it  is  called  acro-parcesthesia. 

We  meet  then  with: 

1.  Cephalic  parsesthesias,  comparable  to  diffuse  headaches. 

2.  Local  parsesthesias,  comparblae  to  local  neuralgias. 

3.  Acro-parsesthesia,  involving  the  feet  or  hands  or  both  diffusely. 

4.  Psychic  and  cerebral  parsesthesias. 

The  cephalic  parsesthesias  are  usually  symptoms  of  neurasthenic 
or  depression  states. 

Acro-parsesthesia  occurs  in  multiple  neuritis,  in  glycosuria,  and  per- 
nicious ansemia. 

Local  forms  affect  the  ulnar,  trigeminal,  cervical,  sciatic  and  lumbar 
nerves  oftenest. 

Under  the  head  of  parsesthesic  neurosis,  the  affection  known  as 
waking  numbness  or  night  palsy  may  be  described.  This  is  a  disorder 
characterized  by  a  temporary  paralysis  of  an  extremity,  with  numbness, 
noticed  on  first  waking  or  after  lying  down  for  a  time.  It  is  a  rare  disease 
and  little  is  known  of  its  cause.  It  occurs  in  adults  and  usually  in  the 
neuropathic.  Sometimes  evidence  of  arthritism,  arterial  sclerosis  or 
poor  innervation  of  the  vessels  is  present. 

The  symptoms  are  much  like  those  caused  by  temporary  compres- 
sion of  a  nerve  when  the  leg  or  arm  goes  to  sleep.     The  paralysis  is 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES 


147 


temporary  and  there  is  no  ansesthesia.     It  is  often  a  very  obstinate 
condition  but  leads  to  no  serious  result. 

In  some  cases  there  is  in  parsesthesia  undoubtedly  a  low  grade  of 
neuritis,  and  in  other  cases  there  is  a  congestion  or  slight  degree  of 
degeneration  of  the  nerve.  Underlying  many  of  the  parsesthesias  of 
middle  and  late  life  is  an  arterial  sclerosis  or  defects  of  metabolism 
with  nerve  degeneration.  Many  of  the  cold  and  heat  sensations  of  this 
period  have  this  vascular  origin,  to  which  is  added  an  undue  mental  ir- 
ritability and  sensitiveness. 

NEURALGIA 

Neuralgia  is  a  condition  characterized  by  pain  in  the  course  of  a 
nerve  or  of  nerves.     It  is  not  a  distinct  disease,  but  only  a  symptom, 


Anxiety  psychosis 


Neurasth 


Eye  strain 
,/_  Neurasthenia 

■--Pelvic  trouble 
Diaphragm 


Fig.  67. — Diagrams  showing  the  distribution  of  the  cerebrospinal  strands  of  nei'ves 
and  the  location  of  transferred  pains  and  neuralgia. 

and  the  tendency  is  to  do  away  with  the  term  except  to  indicate  a  nerve 
pain.     A   large   proportion    of   what   were   formerly    called   neuralgias 


148 


DISEASES    OF    THE    NERVOUS    SYSTEM 


are  due  to  neuritis,  to  some  form  of  organic  disease  or  to  some  reflex 
irritation.  There  is,  however,  a  certain  percentage  of  persistent  nerve 
pains  for  which  we  can  find  no  organic  basis,  and  as  a  matter  of  both 
necessity  and  convenience  we  still  retain  the  word.  We  qualify  it  accord- 
ing to  its  cause  and  its  location.  Hence  we  have  hysterical,  gouty  and 
neuritic  neuralgias,  and  we  have  trigeminal,  cervical,  brachial,  etc., 
neuralgias,  and  we  can  speak  of  neuralgias  as  symptomatic  or  idiopathic 
according  as  we  know  or  do  not  know  the  basis  of  the  trouble.  But 
there  is  little  if  any  idiopathic  neuralgia  for  the  observant  physician. 

The  most  frequent  form  is  the  trigeminal;  next  in  order  come  the 
brachial  and  sciatic. 

Symptoms. — The  dominant  symptom  is  pain.  This  pain  is  sharp, 
darting,    boring,   stabbing   or   burning  in   character.     It   comes   on   in 


Strands  of  Cerebrospinal  Nerves 

Distribution 

Area  1 

Trigeminus,  facial,  etc. 

Face  and  its  orifices,  anterior  scalp. 

Area  11 

Upper  four  cervical. 

Occipital  region,  neck. 

Area  111 

Lower  four  cervical  and  first  dor- 
sal. 
Upper  six  dorsal. 

Upper  extremities. 

Area  IV 

Thoracic. 

Area  V 

Lower  six  dorsal  except  last. 

Abdominal  wall,  upper  lumbar,  up- 
per lateral  thigh  surface. 

Area  VI 

Twelfth  dorsal,  four  lumbar. 

Lumbar  region,  upper  gluteal,  an- 
terior and  inner  thigh  and  knee. 

Area  Vll 

Fifth  lumbar  and  five  sacral. 

Lower  gluteal,  posterior  thigh,  leg. 

paroxysms  of  great  intensity.  In  the  intervals  there  may  be  no  pain 
or  it  may  be  simply  a  dull  ache.  The  pain  runs  along  the  course  of 
certain  nerves,  though  it  is  not  confined  necessarily  to  them,  but  may 
be  somewhat  diffuse. 

The  skin  and  nerves  are  sometimes  tender  or  even  exquisitely  sensi- 
tive. Firm  pressure,  however,  is  usually  not  painful.  In  about  half 
the  cases  of  long  standing,  tender  'points  may  be  found  which  correspond 
to  the  exit  of  nerves  from  a  bony  canal  or  the  substance  of  a  muscle 
or  fascia.  In  rare  cases  there  is  tenderness  over  the  spine  correspond- 
ing to  that  point  where  the  affected  nerves  arise.  Besides  feelings 
of  pain,  there  is  often  a  sense  of  numbness,  cold,  tingling,  or  heaviness 
of  the  limb.  Vasomotor,  secretory  and  trophic  disturbances  may 
occur;  but  when  these  are  pronounced  one  must  suspect  neuritis  or 
an  organic  central  disease.  Muscular  spasm  is  sometimes  present. 
The  paroxysms  of  pain  may  intermit  regularly;  sometimes  they  come  on 
every  day  at  the  same  hour.  They  are  apt  to  be  worse  at  night.  The 
attacks  of  the  disease  often  run  a  course  of  several  weeks  or  months, 
and  in  some  forms  they  last  for  years. 


SENSOEY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         149 

The  painful  sensations  of  neuralgia  usually  originate  in  the  periph- 
eral sensory  neuron.  In  some  cases  as  in  the  neuralgia  of  tabes  and 
perhaps  sometimes  in  tic  douloureaux  and  in  the  herpetic  neuralgias, 
the  posterior  spinal  ganglion  is  chiefly  at  fault;  in  others  the  irritation 
affects  the  entire  sensory  nerve.  The  central  sensory  neurons  that  take 
along  impulses  to  the  brain  are  rarely  the  cause  of  neuralgia,  and  local 
diseases  of  the  cord  and  brain  do  not,  as  a  rule,  cause  pain  bj'-  irritating 
these  sensory  pathways.  Still  there  may  be  neuralgic  pain  from  this 
cause;  and  ''central  nervous  pains"  have  been  observed  in  brain  tumors 
and  after  brain  hemorrhage  or  softening,  when  these  lesions  have  in- 
volved the  posterior  part  of  the  optic  thalamus. 

Pathology. — Many  cases  that  used  to  be  called  neuralgia  are  now 
known  to  be  forms  of  neuritis  or  perineuritis;  e.g.,  sciatica  and  brachial 
neuralgia.  Other  forms  are  sometimes  due  to  impaired  nutrition 
of  the  neuron  from  ah  obliterating  arteritis  (tic  douloureux) ;  still  others 
are  due  to  the  irritation  of  nerves  from  the  diathetic  poison  of  gout, 
rheumatism  and  diabetes,  or  to  extrinsic  poisons,  such  as  alcohol,  lead 
and  arsenic.  In  these  cases  the  sensory  nerves  of  the  nerve-sheaths 
(ne-rvi  nervorum)  are  affected.  There  remain  many  cases  in  which 
the  trouble  shifts  from  one  locality  to  another  or  in  which  no  special 
local  or  general  irritation  can  be  discovered.  In  these  cases  we  assume 
that  the  pathogenic  focus  is  in  the  spinal  or  cerebral  sensory  neurons 
and  is  a  toxaemia  or  a  psychosis. 

There  are  some  forms  of  neuralgia  which  may  be  called  "reminis- 
cent" or  "hallucinatory."  The  patient,  who  is  an  impressionable  and 
sensitive  person,  has  had  a  genuine  cause  for  neuralgic  pains;  but  this, 
after  lasting  some  time,  has  ceased,  while  the  painful  impressions  con- 
tinue to  remain  in  the  cerebral  cortex.  The  neuralgia  is  a  morbid  habit 
of  feeling  pain.  Such  neuralgias  are  promoted  often  by  the  use  of 
morphine.  There  are  neuralgic  pains  occurring  oftenest  in  the  legs, 
but  sometimes  in  the  back,  shoulder  or  arms,  due  to  spasms  of  thickened 
arteries  and  causing  pain  just  as  the  pain  of  angina  pectoris  is  caused. 
These  are  called  anginal  neuralgias.  They  are  often  accompanied  with 
cramping  and  weakness  of  the  muscles. 

Pathogenetically  we  can  divide  neuralgias  into  (1)  toxic;  (2)  ex- 
haustion; (3)  neuritic  and  perineuritic;  (4)  anginal;  (5)  psychic.  Often 
there  is  a  combination  of  these  factors. 

Diagnosis. — This  is  based  on  the  fact  that  neuralgic  pains  are  shift- 
ing, paroxysmal,  follow  the  course  of  nerves,  are  accompanied  often  by 
tender  points  and  not  accompanied  by  signs  of  organic  nerve  disease, 
such  as  paralysis,  anaesthesia  and  tenderness  over  the  nerve-trunk. 
Thermic  sensations  of  burning  or  cold  are  rarely  neuralgic,  but  are  due 
to  neuritis  or  some  organic  change. 


150  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  treatment  will  be  discussed  under  special  heads. 

NEUROSES  OF  THE  NERVES  OF  SPECIAL  SENSE.  THE  OLFACTORY  NERVE 

Anatomy. — -The  olfactory  nerves  consist  of  a  number  of  peripheral  fibres  that  arise 
from  the  olfactory  bulb,  pass  through  the  cribriform  plate  of  the  ethmoid  bone,  and 
are  distributed  to  the  mucous  membrane  of  the  superior  and  middle  turbinated  bones 
and  the  upper  part  of  the  nasal  septum.  The  olfactory  bulb  is  with  its  associated 
parts  really  a  subdivision  of  the  brain  (rhinencephalon)  and  not  a  true  nerve. 

The  central  olfactory  fibres  pass  to  the  hippocampus,  cornu  ammonis,  and  convo- 
lution of  the  corpus  callosum.  Through  cells  in  these  areas  they  are  put  in  connection 
with  the  optic  thalamus  and  with  the  motor  tracts.  The  olfactory  nerves  do  not 
decussate. 


Posterior  superior  lateral  nasal  nerve 
Spheno-palatine  ganglion 


_,.-—  Lateral  nasal  nerve 


External  nasal, 
nerve 


Anterior  palatine  nerve 

Middle  palatine 
Posterior  palatine  nerve- 


Posterior  inferior  nasal  nerve 


|_Lateral 
nasal  nerve 


'■■-  Naso-palatine  nerve 


Posterior  palatine  nerve 

Middle  palatine  lu  i  m 

Anterior  palatine  ner-\  e 

Fig.  68. — Showing  distribution  of  olfactory  and  trigeminal  nerves  in  nose. 

{Cunningham.) 

The  sense  of  smell  is  rudimentary  in  man,  yet  it  is  still  the  sense  by  which  we  can 
appreciate  the  most  attenuated  matter;  for  the  triUionth  of  a  grain  of  mercaptan  is 
able  to  awaken  a  sensation  in  the  mind,  but  has  weight  and  dimensions  so  infinitely 
minute  as  to  be  quite  beyond  the  power  of  the  imagination  to  grasp.  According  to 
Valentin,  we  can  percieve  K200oooofa  grain  of  oil  of  roses.  According  to  Fischer  and 
Penzoldt,  one  can  perceive  >^760000000  of  a  grain  of  mercaptan.  1  have  found  that 
one  can  perceive  the  odor  from  4  cm.  of  a  solution  of  oil  of  cloves,  1  to  100,000. 
Matter  to  be  perceived  as  odor  must  be  in  a  gaseous  form.  Odorous  sensations 
cooperating  with  taste  sensations  form  "flavor."  Variety  in  odorous  sensations 
depends  probably  upon  the  rapidity  of  molecular  vibrations  as  in  the  case  of  light; 


SENSORY    NEUROSES    OF   THE    CEREBROSPINAL    NERVES 


151 


and    substances    having    similar    relations    in    vibration    have    similarity    in    odor 
(Haycraft). 

Anosmia. — The  olfactory  nerve  is  affected  clinically  by  loss  of  func- 
tion, or  anosmia,  increased  sensitiveness  of  function,  or  hyperosmia, 
and  perversions  of  function,  or  parosmia. 

Anosmia  is  far  the  most  common  disorder  of  olfaction. 

Etiology. — Its  usual  cause  is  disease  of  the  mucous  membrane  of 
the  nose.  Injuries,  inflammations  and  tumors  affecting  any  part  of 
the  course  of  the  nerve,  its  bulb  or  central  fibers  may  also  cause  it. 
Unilateral  cortical  lesions  in  the  uncinate  gyrus  may  lead  to  partial 


Fig.  69. 


-Principal  constituent  elements  of  the  olfactory  nerve  of  a  mammal. 

(Van  Gehuchten.)  . 


loss^of  smell.  It  will  be  not  entire,  because  each  nerve  receives  fibres 
from  both  hemispheres.  Paralysis  of  the  fifth  or  seventh  nerve  may 
indirectly  cause  some  anosmia.  Primary  degenerative  changes  due  to 
syphilis  of  the  nervous  system,  as  in  locomotor  ataxia,  and  excessive 
olfactory  stimulation  cause  anosmia.  Anosmia  occurs  sometimes  as 
a  pure  psychosis  in  hysteria,  melancholia  or  in  neurasthenic  states. 
There  may  also  be  a  congenital  absence  of  the  nerves. 

Diagnosis. — This  is  made  by  test  odors.     To  test  the  sense  of  smell, 
a  bottle  of  oil  of  cloves  or  of  some  familiar  non-irritating  odor  may  be 


152  DISEASES    OF    THE    NERVOUS    SYSTEM 

used.  To  detect  quantitative  disturbance  one  may  use  six  phials  con- 
taining oil  of  cloves,  in  purity  and  in  watery  mixture  of  1  to  10,  1  to  100, 
1  to  1000,  1  to  10,000  and  1  to  100,000.  Special  olfactometers  have 
been  devised.  The  sense  of  smell  for  any  single  odor  is  lost  in  about 
three  minutes,  but  returns  after  one  minute's  rest. 

Treatment. — -For  functional  anosmia,  snuffs  containing  strychnine 
gr.  3'^o  S'l^d  gum  acacia  5ij  can  be  used.  Weak  galvanic  and  faradic 
currents  are  recommended.  Usually  there  is  in  anosmia  a  local  diseased 
condition  of  the  nose  which  requires  treatment. 

Hyperosfnia  occurs  only  rarely  and  then  in  neurasthenic,  hysterical 
or  insane  persons.  In  the  latter  it  is  more  often  a  psychical  phenome- 
non than  a  peripheral  disorder.  Hyperosmia  can  be  cultivated,  and 
this  is  done  sometimes  by  the  blind  and  by  those  engaged  in  certain 
pursuits,  such  as  tea  tasting  and  wine  tasting. 

Hallucinations  of  smell  occur  in  the  insane,  as  just  mentioned,  and 
a  few  cases  of  epilepsy  are  reported  in  which  the  aura  was  a  stench. 
In  tumors  of  the  temporal  lobe  irritating  the  olfactory  cortical  centre, 
"stench  seizures"  sometimes  occur.  When  all  olfactory  sensations 
are  disagreeable  the  condition  is  called  kakosmia. 

Parosmia  is  a  not  infrequent  condition.  In  it  everything  smells 
alike  to  the  patient,  or  a  pleasant  odor  is  perhaps  a  peculiar  or  offensive 
one.  This  condition  may  be  due  to  local  disease,  but  is  often  a  symptom 
of  hysteria  or  the  psychoses. 


THE  OPTIC  NERVE 

Anatomy. — The  optic  nerve  is  not  a  true  peripheral  nerve,  but  a  tract  of  the  brain, 
and  it  connects  the  retinal  cells  with  the  brain  proper.  Like  other  brain  tracts,  its 
fibres  have  a  myelin  sheath,  but  no  neurilemma.  The  real  origin  of  the  nerve  is  in 
the  retina,  just  as  the  olfactory  nerve  arises  in  the  peripheral  cells  of  the  olfactory 
mucous  membrane  and  the  spinal  sensory  nerves  arise  in  the  spinal  ganglia. 

The  retina  is  a  nervous  tissue  formed  essentially  of  three  layers  of  nerve-cells. 
From  without  inward  they  are:  the  layer  of  visual  cells,  the  layer  of  bipolar  cells 
and  the  layer  of  ganglionic  cells.  These  different  layers  may  be  subdivided  so  as 
to  give  the  following  layers  from  without  inward: 

1.  The  layer  of  rods  and  cones.   1  „        •       xi     i  j-     •       i      n 

_    „,  ,         ,  ,      ,  f  Jbormmg  the  layer  oi  visual  cells. 

2.  ihe  external  granular  layer.    J 

3.  The  external  molecular  layer.  1  „        •       ^^i     i  i-  i  •     i  n 

.    T  J         1  11  ^  l^ormmg  the  layer  oi  bipolar  cells. 

4.  Internal  granular  layer.  J 

5.  Internal  molecular  layer.  1  Forming   the   layer   of 

6.  Ganglionic  layer,  with  the  fibres  of  the  optic  nerve.     J  ganglion  cells. 

The  layer  of  visual  cells  is  subdivided,  as  seen  in  the  figure,  into  that  of  the  rods 
and  cones  externally  and  that  of  the  external  granular  internally.  This  is,  however, 
practically  a  layer  made  up  simply  of  bipolar  nerve-cells  with  prolongations  more  or 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         153 


sualjield 


less  long  which  run  to  the  external  surface  of  the  retina  and  there  form  a  series  of  bodies 
known  as  the  rods  and  cones. 

In  the  layer  of  bipolar  cells  are  layers  of  cells  with  processes  running  horizontally, 
and  in  the  internal  molecular  layer  are  larger  horizontal  cells,  called  by  Cajal  spongio- 
blasts. There  are  also  in  the  retina  terminal  arborizations  of  cells  whose  origin  is  in 
the  thalamus,  corpora  geniculata,  or  anterior  tubercles.  These  carrj^  impulses  to  the 
retinal  cells. 

The  neuraxons  of  the  ganglionic  cells  send  fibres  which  unite  to  form  the  optic 
nerve. 

The  optic  nerves  each  contain  about  500,000  fibres,  which  is  about  the  same  as 
the  total  of  all  the  sensory  fibres  of  the  spinal  nerves.  They  pass  to  the  optic  chiasm, 
where  about  one-third  of  the  fibres  cross,  in 
man.  In  lower  animals  the  decussation  is 
greater.  Those  fibres  which  do  not  cross  come 
from  the  outer  or  temporal  third  of  the  retina; 
those  which  do  cross  come  from  the  internal 
or  nasal  two-thirds.  A  few  fibres  pass  from 
one  optic  centre  of  the  brain  along  the  poste- 
rior border  of  the  optic  chiasm  to  the  centre  of 
the  opposite  side  (commissure  of  Gudden). 
After  leaving  the  chiasm,  the  fibres  form  the 
oftic  tract.  The  tract  curves  up  and  back 
around  the  crus  cerebri,  and  divides  into  a  lat- 
eral and  mesial  root. 

These  roots  connect  with  the  external 
geniculate  body,  the  anterior  tubercles  of  the 
corpora  quadrigemina  and  the  posterior  gan- 
glion of  the  thalamus,  i.e.,  the  pulvinar.  These 
ganglia  are  called  the  primary  optic  centres. 
Through  the  anterior  tubercles  of  the  corpora 
quadrigemina  and  by  other  means,  the  optic 
nerve  is  connected  with  the  oculo-motor  nerve, 
and  thus  reflex  movements  of  the  pupils,  lids 
and  eyeballs  are  brought  about. 

From  these  primary  optic  centres,  fibres 
enter  the  posterior  part  of  the  internal  capsule, 
curve  up  and  back  toward  the  occipital  lobes, 
forming  the  optic  radiations  of  Gratiolet.     The 

inferior  longitudinal  bundle  is  part  of  these  radiations  and  connects  the  external 
geniculate  body  with  the  calcarine  cortex  (A.  Meyer). 

They  are  finally  distributed  to  the  cortex  of  the  occipital  lobe,  and  in  man  chiefly 
to  the  cuneus  and  the  parts  about  the  calcarine  fissure. 

It  will  be  seen  that  each  retina  is  connected  with  the  occipital  lobe  of  both 
hemispheres;  further,  that  the  outer  or  temporal  half  of  each  retina  is  connected 
with  the  occipital  lobe  of  the  same  hemisphere,  and  the  inner  or  nasal  half  of  each 
retina  with  the  occipital  lobe  of  the  opposite  side.  The  upper  part  of  each  retina 
seems  to  be  connected  with  the  lower  part  of  the  cuneus,  and  vice  versa  (Fig.  70). 

Other  associations  exist  by  which  the  optic  centres  on  the  two  sides  are  connected 
with  each  other  and  with  other  cranial  nerves  in  the  medulla. 

The  optic  nerve  is  a  nerve  of  special  sense  of  vision  and  has  no  other  function  ex- 
cept that  of  an  oxcito-reflex  character. 


Fig.  70. — Showing  relation  of 
occipital  cortex  and  its  visual  cen- 
tres to  the  eye  and  visual  fields. 
{Bing.) 


154 


DISEASES    OF    THE    NERVOUS    SYSTEM 


DISEASES  OF  THE  OPTIC  NERVE 

The  optic  nerve  may  be  affected  by  nearly  all  forms  of  pathological 
change.  For  the  neurologist,  however,  the  especially  important  con- 
ditions are  inflammations,  degenerations,  injuries  and  functional  dis- 
orders. Inflammation  of  the  nerve,  or  optic  neuritis,  may  occur  as 
a  papillitis  or  inflammation  of  the  head  of  the  nerve,  a  neuro-retinitis  or 
descending  neuritis,  or  a  retro-bulbar  neuritis.  Perineuritis  is  rare. 
Neuro-retinitis  and  papillitis  are  closely  associated  clinically  and  patho- 
logically (Noyes),  so  that  practically  only  two  forms  of  neuritis  need  be 
discussed  separately. 

Papillitis  and  Neuro-retinitis — Etiology. — This  condition  is  seen  by 


'<Co8^ 


Fig.  71. — The  optic  nerve  showing  detail  of  the  primary  optic  centers.     {Cunningham.) 

neurologists  in  connection  with  brain  tumors,  brain  abscess,  meningitis 
and  occasionally  multiple  neuritis.  The  other  causes  are  nephritis, 
diabetes,  infectious  fevers,  lead,  and  severe  hemorrhages.  The  disease 
occurs  at  all  ages  and  in  both  sexes.  In  brain  tumors  it  occurs  in  two- 
thirds  of  the  cases,  and  especially  often  in  cerebellar  tumors.  It  occurs 
in  80  per  cent,  of  cases  of  tuberculous  meningitis. 

Symptoms. — -Subjective  symptoms  are  often  not  present.  The 
vision  may  remain  good  for  a  long  time.  In  other  cases  there  are  con- 
centric limitation  of  the  vision  field,  loss  of  color  sense,  and  scotomata. 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         155 

For  a  description  of  opthalrnoscopic  changes  the  reader  is  referred  to  a 
special  text-book.  It  is  in  this  condition  that  "choked  disc,"  which  is  a 
papillitis  with  much  serous  infiltration,  occurs.  The  changes  are  less 
striking  in  neuro-retinitis.  The  disease  may  affect  one  or  both  nerves. 
In  brain  disease  both  nerves  are  usually  involved. 

Pathology  and  Pathological  Anatomy. — The  process  is  usually  sub- 
acute or  chronic.  Congestion,  exudation,  small  hemorrhages  and 
collections  of  leukocytes  occur.  The  sheath  of  the  nerve  just  back 
of  the  globe  is  often  distended  with  a  serous  exudate.  After  a  time  the 
nerve-fibres  atrophy,  connective  tissue  proliferates  and  takes  their  place, 
and  we  have  a  secondary  optic  atrophy. 


Fig.  72. — Neuro-retinitis.     {Jaeger.) 

The  process  is  essentially  peripheral,  but  it  extends  back  with  lessening 
intensity  into  the  trunk  of  the  nerve.  The  purely  mechanical  theory  of 
neuritis,  that  it  is  due  to  compression,  can  be  accepted  only  in  some  cases. 
It  is  probable  that  the  neuritis  results  from  an  irritating  serous  fluid 
which  extends  down  the  sheath  of  the  nerve,  this  sheath  being  a  prolonga- 
tion of  the  arachnoid  cavity.  Mechanical  causes  lead  to  constriction, 
accumulation  of  the  fluid,  and  compression  of  the  nerve  at  its  periphery, 
and  hence  to  inflammation.  Sometimes,  at  least,  the  irritating  fluid 
contains  microbes  or  microbic  poisons.     (See  also  Brain  Tumors.) 

Retrobulbar  Neuritis. — In  this  disease  the  lesion  lies  chiefly  behind 
the  globe.  Its  causes  are  especially  toxaemia  from  alcohol  and  tobacco. 
It  is  also  due  to  rheumatic  toxins,  syphilis,  lead  and  diabetes. 

In  the  acute  cases  there  is  usually  rather  rapid  loss  of  sight,  with 
some  pain  and  tenderness.     The  ophthalmoscopic  changes  are  relatively 


156  DISEASES    OF    THE    NERVOUS    SYSTEM 

slight.  In  chronic  cases,  which  are  usually  toxic  in  origin  and  due  to 
alcohol  or  tobacco,  or  oftenest  to  both;  there  are  color  scotomata  or 
absolute  scotomata  and  amblyopia.  There  is  no  pain.  The  condition 
is  known  as  tobacco  or  alcoholic  amblyopia. 

The  -prognosis  of  neuritis  varies  with  the  cause.  If  this  is  removable, 
as  in  the  toxaemias,  recovery  is  the  rule.  This  is  a  proof  that  in  neuritis 
the  connective  tissue  is  the  part  chiefly  involved,  for  a  destroyed  or 
atrophied  optic  nerve  does  not  recover.  In  many  cases,  however, 
atrophy  follows  the  neuritis. 

The  treatment  is  based  on  the  cause.  One  may  need  to  use  cups, 
salicylates,  the  iodides  and  mercury  and  salvarsan;  later,  the  iodides 
and  strychnine.      The  rhinologist  and  surgeon  may  be  needed. 


Fig.  73.— "Choked  disc." 

Degeneration  of  the  Optic  Nerve,  or  Optic  Atrophy.— This  condition 
may  be  primary  or  secondary.  Secondary  atrophy  is  usually  the  results 
of  a  neuritis.     I  shall  describe  here  primary  optic  atrophy. 

Etiology .^ — It  occurs  oftener  in  men  than  in  women  (three  to  one). 
It  may  be  hereditary;  it  may  be  the  result  of  some  toxin;  but  practically, 
it  is  usually  due  to  syphiHs  and  appears  in  tabes  or  paresis.  It  occurs 
in  multiple  sclerosis  and  hereditary  ataxia.  It  may  occur  apparently 
as  a  simple  primary  affection,  though  these  cases  are  generally  optic 
forms  of  tabes  dorsalis. 

The  symptoms  are  those  of  gradual  decrease  of  acuity  of  vision,  con- 
centric limitation  of  the  visual  field,  loss  of  color  sense,  dilatation  and 
immobility  of  the  pupil.  The  sense  of  sight  may  remain  good  for  a  long 
time.     Ophthalmoscopically,  the  nerve  disc  is  opaque,  grayish,  or  dirty- 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         157 

looking,  and  often  has  a  cup-shaped  or  "cupped-disc"  appearance.  The 
vessels  are  smaller  and  few  in  number. 

The  pathology  and  pathological  anatomy  are  that  of  a  parenchy- 
matous degeneration  with  loss  of  nerve-fibres,  which  are  replaced  by 
connective  tissue. 

The  prognosis  is  almost  uniformly  bad. 

The  treatment  is  that  usually  of  the  cerebral  or  spinal  disease.  Mer- 
cury, iodides,  strychnine,  phosphorus  and  iron  are  given.  Warm  baths 
and  salicylate  of  soda  sometimes  have  a  temporarily  good  effect.  Strych- 
nine in  physiological  doses  gives,  however,  the  best  symptomatic  results. 
Electricity  is  not  of  any  use.  Stretching  the  nerve  does  no  good.  In- 
jections of  salvarsan  have  sometimes  been  efficient. 

The  optic  nerves  and  their  primary  and  cortical  centres  are  subject 
to  various  other  diseases.  So  far  as  these  are  organic,  they  will  be  de- 
scribed in  detail  under  the  head  of  brain  diseases.  But  there  are  certain 
symptoms  often  of  functional  origin  which  are  best  described  here. 
These  are:  (1)  Amblyopia  and  amaurosis;  (2)  retinal  hyperesthesia  and 
dyssesthesia;  (3)  hemianopsia. 

Amblyopia  and  Amaurosis. — Amblyopia  is  a  partial  loss  or  dimness 
of  vision,  there  being  no  observable  lesion  of  the  eye,  or  its  nerves. 
Amaurosis  is  a  total  loss  of  vision,  also  without  observable  lesion. 

The  causes  are  shocks,  hysteria,  migraine,  concussion  of  the  brain, 
and  severe  hemorrhages.  There  are  also  certain  toxic  causes,  chiefly 
alcohol  and  tobacco,  quinine,  and  salicylic  acid.  Other  causes  are 
arterial  sclerosis  and  renal  disease  leading  to  spasm  of  the  retinal  vessels 
or  of  those  of  the  occipital  cortex.  Night  blindness  and  snow  blindness 
are  forms  of  functional  amblyopia. 

The  symptoms  are  diminution  or  loss  of  vision,  usually  sudden, 
temporary  and  involving  both  eyes.  Amblyopia  in  hysteria  is  usually 
greater  in  one  eye  and  associated  with  concentric  limitation  of  the  visual 
field  and  disturbance  of  color  sense. 

Underlying  amblyopia  there  may  be  minute  hemorrhages  in  the 
brain,  causing  temporary  pressure,  or  a  vascular  spasm,  causing  anaemia. 

Retinal  or  ocular  hypercesthesia  is  a  condition  in  which  the  eye  is 
abnormally  sensitive  to  light.  It  may  be  due  to  exposure  to  extreme 
light  or  to  seclusion  in  a  dark  room.  The  neurologist  sees  it  oftenest 
as  a  symptom  of  hysteria  {vide  Hysteria)  and  neurasthenia.  It  occurs 
in  mydriasis  and  albinism.  It  is  not  to  be  confounded  with  photophobia 
due  to  irritation  of  the  conjunctiva. 

Nyctalopia,  or  the  condition  of  seeing  better  in  a  dim  light,  is  a 
form  of  the  disease. 

Hemianopsia,  or  half-sightedness,  or  hemianopia,  a  condition  in 
which  there  is  a  blindness  of  one-half  the  visual  field,  may  be  due  to  a 


158  DISEASES    OF    THE    NERVOUS    SYSTEM 

functional  or  organic  disorder  of  the  nerve  or  its  centres.  It  is  a  symp- 
tom of  many  lesions  and  conditions,  and  can  be  described  only  generally 
here. 

Etiology. — Its  principal  functional  cause  is  migraine.  Its  organic 
causes  are  tumors,  inflammations,  softenings  or  hemorrhages  involving 
part  of  the  optic  nerve  or  its  central  connections. 

Symptoms. — Various  descriptive  terms  are  used  to  indicate  the 
character  of  the  hemianopsia.  In  lateral  hemianopsia  a  vertical  half 
of  the  field  is  involved.  In  lateral  homonymous  hemianopsia  there 
is  half-blindness  on  the  left  or  right  side  of  each  eye,  as  the  case  may  be. 
In  temporal  hemianopsia  the  outer  halves  of  the  eyes,  and  in  nasal 
the  inner  halves,  are  involved.  The  upper  or  lower  segments  or  irregu- 
lar segments  of  the  visual  field  may  be  involved. 

These  various  forms  of  hemianopsia  depend  upon  the  location  of 
the  lesion  which  cuts  into  and  destroys  the  optic  fibres  in  their  course 
from  the  eye  to  the  visual  centre  in  the  occipital  cortex.  The  mechanism 
will  be  understood  when  it  is  remembered  that  each  occipital  lobe  is 
supplied  by  nerve-fibres  from  one-half  of  the  retina  of  each  eye.  A  cut 
shows  this  better  than  any  description  (Figs.  70,  71).  In  binasal  hemian- 
opsia the  lesion  must  be  in  front  of  or  practically  directly  on  the 
chiasm.  In  bilateral  temporal  hemianopsia  it  must  be  double  and  at 
each  side.  In  lateral  hemianopsia  the  lesion  must  lie  farther  back  than 
the  chiasm,  in  the  tract,  the  primary  centres,  the  optic  radiations  or 
occipital  lobes. 

In  hemianopsia  from  disease  of  the  nerve  as  far  back  as  and  includ- 
ing the  primary  centres  in  the  optic  thalamus  and  corpora  quadrigemina 
there  is  a  loss  of  light  reflex  when  a  ray  of  light  is  thrown  upon  the  blind 
side  of  the  retina,  but  the  pupil  still  contracts  when  light  is  thrown  on  the 
sensitive  side  of  the  retina.  This  phenomenon  is  called  "Wernicke's 
hemiopic  pupillary  reaction."  If  in  hemianopsia  the  light  reflex  is  pre- 
served, the  lesion  is  back  of  the  primary  centres  and  involves  the  optic 
radiations  or  cortex.     The  test  can  only  be  made  with  special  apparatus. 

A  test  for  the  condition  of  hemianopsia  in  its  early  stage,  and  one 
that  is  useful  in  stupid  or  partially  comatose  patients,  is  the  following: 
When  the  finger  is  suddenly  brought  in  front  of  the  eye  on  the  sound 
side,  there  is  a  wink ;  if  brought  in  front  from  the  blind  side,  the  orbicularis 
does  not  contract. 

Hemianopsia  is  almost  always  the  sign  of  organic  disease.  It  is  not 
found  in  hysteria,  but  does  occur  in  migraine.  It  is  best  made  out  and 
recorded  by  means  of  the  perimeter. 

Its  course  and  treatment  depend  upon  the  cause. 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES 


159 


SENSORY  NEUROSES  OF  THE   TRIGEMINAL  NERVE 

Anatomy. — The  trigeminus  or  fifth  nerve  is  one  of  the  most  extensively  distributed 
and  most  delicately  sensitive  nerves  of  the  body.  Its  sensory  branches  represent  the 
atrophied  and  lost  sensory  roots  of  the  third,  fourth,  sixth,  seventh  and  twelfth  cranial 
nerves.  The  trigeminal  nerve  is  a  mixed  nerve.  It  has  two  nuclei  of  origin;  a  central 
nucleus  for  the  motor  part  and  a  peripheral  nucleus  for  the  sensory  part.  The  motor 
nucleus  has  two  parts :  a  chief  nucleus  lying  deeply  in  the  substance  of  the  pons  Varolii, 
and  an  accessory  nucleus,  which  consists  of  a  long  tract  of  gray  matter,  known  as  the 
descending  root  and  lying  in  the  upper  part  of  the  dorsal  portion  of  the  pons.  It 
passes  down  along  the  side  of  the  aqueduct  of  Sylvius.  The  sensory  root  of  the  tri- 
geminal has  its  origin  in  the  Gasserian  ganglion,  which  is  composed  of  unipolar  cells,  like 
those  of  the  spinal  ganglia.  The  axis-cylinder  processes  of  these  cells  bifurcate;  the 
external  branches  pass  outward  and  become  part  of  the  peripheral  sensory  nerve,  the 


Fig.  74. — Showing  the  origin  of  the  cranial  nerves  and  the  extent  of  the  origin  of 

the  trigeminus.      (Edinger.) 


internal  branches  pass  into  the  substance  of  the  pons,  and  there  give  off  ascending  and 
descending  branches.  The  ascending  branches  are  short,  and  pass  to  a  terminal 
nucleus,  known  heretofore  as  the  sensory  nucleus  of  the  trigeminus.  The  descending 
branches  pass  down  to  the  pons  and  medulla,  as  far  as  the  cervical  part  of  the  spinal 
cord  and  form  the  ascending  root  of  the  trigeminus. 

The  nuclei  of  the  trigeminus  reach  the  whole  length  of  the  pons  and  medulla, 
and  are  co-extensive  with  the  origin  of  all  the  other  cranial  nerves  (Fig.  74).  Hence 
the  frequency  with  which  its  disorders  are  complicated  with  those  of  these  nerves.  Its 
cortical  origin  is  probably  in  the  lower  part  of  the  post-central  convolution. 

The  trigeminus  supplies  sensation  to  the  face,  conjunctivae,  nose,  the  frontal  and 
maxillary  sinuses,  the  teeth,  the  palate,  tongue  and  part  of  the  upper  pharynx;  also 
to  the  scalp  as  far  back  as  the  vertex  and  to  the  external  auditory  meatus  (Fig.  75). 
The  distribution  is  not  always  the  same  and  is  helped  by  fibres  from  the  cervical  nerves. 

It  gives  sensation  also  to  the  anterior  three-fourths  of  the  dura  mater,  the  falx  and 
probably  the  tentorium.  The  pia  and  arachnoid  are  not  sensitive.  The  posterior 
fossa  and  the  occipital  part  of  the  dura  mater  are  supplied  by  the  vagus.  The  tri- 
geminus also  supplies  the  above-named  parts  with  trophic,  vasomotor  and  secretory 
fibres.  The  vasomotor  fibres  are  brought  to  it,  in  part,  from  the  medulla  and  cervical 
spinal  cord  via  the  sympathetic;  the  secretory  fibres  have  the  same  origin.  An  excep- 
tion is  to  be  made  of  the  lachrymal  secretory  fibres  which  are  brought  by  the  motor 
nerves  of  the  eyeball.     The  opinion,  based  largely  on  physiological  experiment,  that 


160 


DISEASES    OF    THE    NERVOUS    SYSTEM 


the  trigeminus  sends  trophic  fibres  to  the  conjunctivae  and  cornea  is  apparently  con- 
tradicted by  the  many  successful  cases  of  entire  extirpation  of  the  Gasserian  ganglion 
without  any  inflammation  of  the  eye  following. 

The  trigeminus  supplies  motion  to  the  muscles  of  mastication,  viz., 
the  two  pterygoids,  the  temporal,  masseter,  mylo-hyoid  and  anterior 
belly  of  the  digastric.  The  sensory  neuroses  of  this  nerve  are  neuralgia, 
parsesthesia  and  anaesthesia. 

Neuralgias  of  the  Trigeminus. — The  trigeminal  nerve  is  subject  to 
two  types  of  neuralgia,  viz.:  (1)  The  symptomatic  pains;  (2)  tic  dou- 
loureux. 


Fig.  75. — Showing  the  distribution  of  the  sensory  nerves  of  the  face.  I,  II,  III, 
First,  second,  and  third  branches  of  the  fifth.  The  shaded  part  is  supplied  by  the 
cervical  nerves;  2  C.a.br.,  second  cervical  anterior  branch;  2  C.p.hr.,  second  cervical 
posterior  branch. 

1.  The  symptomatic  pains  are  by  far  the  most  frequent. 

They  may  be  supra-orbital,  infra-orbital  or  supra-maxillary,  in- 
fra-maxillary or  dental,  and  mixed  forms.  The  most  common  type  is 
the  supra-orbital;  next,  the  mixed  form. 

Etiology. — The  female  sex  is  oftenest  affected;  most  cases  are  seen 
in  the  first  half  of  life;  most  attacks  occur  in  the  winter  and  spring. 
The  left  side  is  oftener  affected.  The  second  and  third  branches  of 
the  fifth  nerve  are  most  susceptible  to  rheumatic  influences,  the  first 
branch  to  malarial  and  septic  poisons.  Dental  disorders  naturally 
are  frequent  factors  in  neuralgia  of  the  second  and  third  branches. 
Exposure,  infections  and  other  depressing  influences  are  factors  in  caus- 
ing these  neuralgias.  Ocular,  nasal,  antrum  and  frontal  sinus  disease 
may  cause  pain  in  the  supra-orbital  nerve.     Syphilis,  malaria,  hysteria, 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         161 

epilepsy,  trauma,  rheumatism,  tumors,  bony  disease  all  may  be  factors 
in  causing  trigeminal  pains.     It  is  sometimes  due  to  herpes  zoster. 

Symptoms. — The  pains  of  trigeminal  irritation  are  sharp  and  in- 
tense, with  exacerbations  and  remissions.  Their  character  and  duration 
depend  on  the  cause.  There  is  no  specific  disease  to  describe  (see 
migraine  and  headache). 

Tic  Douloureux  (Prosopalgia,  FothergilVs  Neuralgia,  Epileptiform 
Neuralgia). — Tic  douloureux  is  a  special  form  of  trigeminal  neuralgia 
occurring  in  middle  or  advanced  life,  unusually  severe  in  its  symptoms 
and  obstinate  in  its  course.  It  ought  to  be  distinguished  sharply  from 
the  ordinary  forms  of  trigeminal  neuralgia.  These  latter  are  sympto- 
matic pains  almost  altogether;  while  tic  douloureux  is  a  special  dis- 
order, dependent  upon  changes  in  the  nerve  itself. 

Etiology. — It  occurs,  as  a  rule,  in  persons  who  are  over  forty,  and 
is  seen  in  the  very  aged.  It  is,  indeed,  almost  the  only  neuralgia  which 
old  people  have.  It  occurs  in  men  and  women  in  about  equal  frequency. 
It  is  brought  on  by  exposure,  overwork  and  depressing  influences;  some- 
times, perhaps,  by  local  diseases  of  the  teeth,  antrum  and  jaws.  There  is 
almost  always  decided  evidence  of  arterial  sclerosis. 

Symptoms. — It  is  characterized  by  intense  darting  pains,  which 
usually  start  in  the  upper  lip  and  by  the  side  of  the  nose.  From  here 
they  radiate  through  the  teeth  or  into  the  eye  and  over  the  temple,  brow 
and  head.  They  are  confined  to  one  side  of  the  head.  During  a  par- 
oxysm the  face  usually  flushes,  the  eyes  water,  the  nose  runs  and  the 
patient  assumes  an  expression  of  the  greatest  agony.  The  attack  lasts 
for  a  few  minutes,  then  becomes  somewhat  less,  and  the  pain  may 
cease  entirely.  A  breath  of  cold  air,  speaking,  eating,  putting  out  the 
tongue — all  bring  on  paroxysms.  The  pains  are  worse  in  winter  and 
often  become  less  or  cease  during  summer.  Occasionally  they  come  on 
for  a  few  months  every  year,  usually  during  the  spring.  The  pains 
are  always  limited  to  one  side  of  the  face  and  are  centred  chiefly  in  one 
branch  of  the  nerve  oftenest  in  the  supra-maxillary  and  next  in  the  infra- 
maxillary.  They  may  spread  so  as  to  involve  the  whole  of  one  side  of 
the  face  and  tongue. 

Spasmodic  movements  of  the  face,  tongue  or  jaws  may  be  associated 
with  the  pain. 

Examination  rarely  reveals  any  objective  trouble,  but  in  a  few  cases 
some  anaesthesia  may  be  noted.  The  disease  causes  loss  of  sleep  and 
impairment  of  nutrition  through  the  pain  caused  by  eating.  Much 
depression  of  spirits  naturally  exists,  for  the  pain  is  the  worst  agony 
that  nature  in  a  hellish  mood  could  devise.  There  is  a  tendeney  to 
a  cure,  however,  and  some  patients  get  well  spontaneously  in  from 
seven  to  fifteen  years. 
11 


162  DISEASES    OF    THE    NERVOUS    SYSTEM 

Pathology. — The  disease  is  usually  a  degenerative  one,  and  prob- 
ably is  due  to  irritative  and  atrophic  processes  occurring  in  the  nerve 
and  its  ganglion.  A  low  grade  of  neuritis,  perhaps  from  alveolar  dis- 
ease, has  been  found  sometimes,  but  as  a  rule  the  nerve  does  not  appear 
much  changed.  The  arteries  supplying  the  nerve,  however,  often 
undergo  the  changes  of  endarteritis,  their  calibre  is  much  lessened,  and 
the  nerve  cannot  get  its  proper  supply  of  blood.  Thus  an  obliterative 
arteritis  underlies  some  cases  of  the  disease.  The  ganglion  shows 
sometimes  evidences  of  degenerative  changes,  but  these  must  usually 
be  considered  secondary,  for  division  of  the  nerve  almost  invariably 
stops  the  pain  for  one  or  two  years  at  least.  On  the  whole,  the  most 
satisfactory  view  of  the  pathology  as,  I  first  showed,  is  that  the  neuralgia 
is  due  to  an  obliterating  neuritis  causing  a  defective  nutrition  of  the 
nerve  and  accompanied  with  vascular  spasm.  Tic  douloureux  is  a  kind 
of  trigeminal  angina. 

Some  cases  occurring  in  younger  people  are  explained  by  the  presence 
of  distinct  local  disease  and  a  hysterical  pain  habit. 

Treatment. — In  cases  which  occur  in  old  people,  the  use  of  nitro- 
glycerin given  in  doses  of  gr.  j-^oo  q-  2  h.  sometimes  has  a  happy  effect. 
An  occasionally  good  remedy  is  crystalline  aconitia  given  in  doses  of 
3^00  gr-  until  its  physiological  effect  is  obtained.  Quinine,  gelsemium, 
croton  chloral  and  codeine  may  be  found  useful.  The  common  practice 
of  pulling  out  all  the  teeth  is  almost  always  unsuccessful,  and  ought  not 
to  be  undertaken  without  specially  good  reason.  Tonics  containing  iron, 
phosphorus,  quinine  or  arsenic  are  generally  helpful.  In  younger  patients 
the  remedies  recommended  under  the  head  of  migraine  and  headache 
may  be  given.  Change  to  a  warm,  equable  climate  may  be  tried;  it  is 
not  a  certain  resource. 

I  have  found  that  in  cases  not  of  over  four  or  five  years'  duration, 
rest  in  bed  with  massive  doses  of  strychnine  often  effects  striking  cures. 
The  drug  should  be  given  hypodermatically  in  doses  of  gr.  3^o  once, 
or  better  three  times,  daily,  gradually  and  very  slowly  increased  until 
gr.  3^  or  3^:5  three  times  a  day  is  reached.  This  is  repeated  four  days 
and  then  the  amount  gradually  reduced.  The  whole  treatment  takes 
about  six  weeks.  The  patient  must  be  kept  rigidly  quiet  in  bed  or  in  the 
bed-room  and  the  full  course  persisted  in.  After  finishing  the  strychnia, 
iodide  of  potassium  and  iron  are  given.  The  treatment  may  have  to  be 
repeated  with  lessened  rigor.  The  treatment  by  large  doses  of  opium, 
gr.  iii.  to  vi.  daily,  is  uncertain  and  often  dangerous.  Sometimes  massive 
doses  of  quinine  break  up  an  attack. 

Finally,  surgical  interference  may  be  necessary.  The  removal  of  the 
nerve  at  as  deep  a  point  as  possible  is  the  only  operation  to  be  seriously 
entertained.     This  sometimes  causes  cure,  but,  as  a  rule,  the  pain  comes 


SENSORY   NEUROSES    OF   THE    CEREBROSPINAL   NERVES        163 

back  in  six  months  to  a  few  years.  Even  such  a  respite,  however,  is 
often  gladly  seized  upon.  Removal  of  the  Gasserian  ganglion  has  been 
attempted  with  success.  There  are  numerous  methods  of  operating 
upon  the  different  branches  of  the  trigeminus  and  resecting  it  distal 
to  the  ganglia. 

Hartley,  of  New  York,  has  devised  an  operation  by  which  he  enters 
the  middle  fossa  through  an  opening  in  the  temporal  bone,  thus  reaching 
the  root  of  the  nerve.  Abbe  has  modified  it  very  successfully.  He 
trephines  the  skull,  enters  the  middle  fossa,  cuts  off  the  second  and  third 
nerve-roots  and  plugs  the  foramen  ovale.  The  operation  in  proper 
hands  is  safe  and  most  efficient.  Injection  of  the  Gasserian  ganglion 
with  alcohol  introduced  by  a  needle  passed  through  the  cheek  and 
upward  behind  the  jaw  through  the  foramen  ovale  is  an  operation  which 
has  been  successful.  Injections  of  alcohol  are  also  made  into  the 
different  branches  of  the  nerve.  The  treatment  is  a  safe  one  and  pro- 
duces often  temporary  good  results.  On  the  whole  it  is  a  rather  disap- 
pointing procedure. 

Trigeminal  Paraesthesia. — Sometimes  persons  suffer  from  peculiar 
numbness,  thrilling  or  formication  in  the  course  of  the  trigeminus.  The 
sensation  may  be  nearly  constant  and  excessively  annojdng.  It  never 
amounts  to  actual  pain.  It  occurs  in  anaemic,  nervous  and  hys- 
tei'ical  persons.  It  may  follow  an  attack  of  herpetic  neuralgia  of  the 
face.  It  is  to  be  regarded  as  an  abortive  form  of  neuralgia  or  neuritis 
and  so  treated. 

Trigeminal  Anaesthesia. — ^This  occurs  from  various  pathological 
lesions  in  the  course  of  the  nerve  or  in  its  nuclei.  The  most  common 
organic  causes  are  brain  tumors,  syphilitic  disease  of  the  membranes  at 
the  base  of  the  brain,  and  herpes.  Trigeminal  anaesthesia  occurs  together 
with  anaesthesia  of  other  areas  in  hysteria  and  in  organic  disease  of 
the  nerve-centers.  It  is  sometimes  noted  in  tic  doloureux  and  facial 
hemiatrophy. 

Flushing,  pallor,  lacrymation,  salivation,  are  all  symptoms  of  disturb- 
ance of  the  trophic,  vasomotor  and  secretory  fibres  running  in  the  tri- 
geminal nerve.  They  are  usually,  if  pathological,  only  concomitant 
symptoms  of  other  diseases. 

Facial  herpes  may  occur  due  to  an  inflammation  of  the  Gasserian 
ganglion,  and  it  is  accompanied  with  much  pain  followed  by  cutaneous 
anaesthesia  and  paraesthesia,  but  it  is  a  malady  generally  belonging  to 
internal  medicine  or  dermatology. 

HEADACHE  (CEPHALALGIA) 

Headache  is  the  name  given  to  attacks  of  diffuse  pain  affecting 
different  parts  of  the  head  and  not  confined  to  the  tract  of  a  particular 


164  DISEASES    OF    THE    NERVOUS    SYSTEM 

nerve.  It  usually  comes  on  in  paroxysms  at  various  intervals,  but  may  be 
continuous. 

Etiology. — Headache  is  the  most  common  of  nervous  symptoms. 
Ten  to  fifteen  per  cent,  of  school-children,  twenty-five  per  cent,  of  men, 
and  over  fifty  per  cent,  of  women  are  subject  to  it,  more  or  less,  though 
this  proportion  would  be  much  reduced  if  migraine  were  excluded  from 
statistics. 

The  headache  ages  are  from  ten  to  twenty-five  and  thirty-five  to 
forty-five;  most  cases  occur  between  the  ages  of  eight  and  twenty-five, 
especially  in  females.  The  number  of  headaches  increases  gradually 
from  the  period  five  to  ten  years  up  to  the  period  fifteen  to  twenty,  then 
falls  until  the  thirty-fifth  year,  and  rises  again  until  about  the  age  of  forty. 
Early  childhood  and  decHning  age  are  practically  exempt  from  chronic 
functional  headaches.  Women  suffer  from  it  more  than  men  in  the 
proportion  of  about  three  to  one.  It  is  more  frequent  in  city  populations 
and  among  the  wealthier  classes.  Headaches  are  more  common  in  the 
spring  and  fall  and  in  temperate  chmates.  Headaches  may  be  classed,  in 
accordance  with  their  causes,  as  follows: 

1.  Exogenous  and  endogenous  toxaemias,  in  which  impoverished 
or  disordered  blood  is  brought  to  the  brain,  as  in  (a)  gastro-intestinal 
disorders;  (6)  diathetic  states:  gout,  rheumatism,  uraemia;  (c)  infections: 
malaria,  fevers. 

2.  Toxic  causes:  lead,  alcohol,  tobacco,  etc. 

3.  Neuropathic  states:  epilepsy,  neurasthenia,  hysteria. 

4.  Reflex  causes:  ocular,  nasopharyngeal,  auditory,  gastric,  sexual. 

5.  Organic  disease,  including  arteriosclerosis,  syphihs,  tumors, 
neuritis,  meningitis  and  diseases  of  the  cranial  bones.  Very  frequently 
several  causes  act  together.  The  autotoxic,  dyspeptic,  ocular  and 
neurasthenic  are  the  common  forms  of  chronic  and  recurrent  headache. 

Edinger  thinks  that  a  large  percentage  of  chronic  headaches  is  due  to 
the  presence  of  certain  nodules  of  rheumatic  or  myositic  origin  situ- 
ated near  the  origin  of  the  muscles  of  the  back  of  the  head.  Mas- 
sage by  removing  these  relieves  the  headache.  I  have  not  found 
these  often,  and  doubt  if  they  have  so  much  importance,  but  their 
existence  and  possible  influence  should  be  borne  in  mind,  especially  in 
gouty  subjects. 

Symptomatology. — ^Headaches  may  be  classed  in  accordance  with  their 
location  and  the  character  of  the  pain.  We  have  accordingly:  (1) 
frontal  headaches;  (2)  occipital  headaches;  (3)  parietal  and  temporal 
headaches;  (4)  vertical  headaches;  (5)  diffuse  headaches  and  various 
combinations  of  the  above. 

The  most  common  form  of  headache  is  the  frontal,  next  the  fronto- 
occipital  or  diffuse,  next  the  occipital. 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES 


165 


The  kind  of  pain  differs  with  different  persons  and  with  different 
causes.  We  have:  (1)  pulsating,  throbbing  headache;  (2)  dull,  heavy 
headache;  (3)  constrictive,  squeezing,  pressing  headache;  (4)  hot, 
burning,  sore  sensations;  (5)  sharp,  boring  pains. 

The  first  form  characterizes  headaches  with  vasomotor  disturb- 
ances, and  usually  indicates  migraine  (throbbing  headache).  The 
second  is  usually  of  a  toxic  or  dyspeptic  type  (the  dopey  headache). 
The  third  is  found  in  the  neurotic  and  neurasthenic  (the  pressure  head- 
ache). The  fourth  in  rheumatic  and  anaemic  cases.  The  fifth  in 
hysterical,  neurotic  and  epileptic  cases. 

Cerebral  congestion. — Anxiety  neurosis 


Neurosthenia 
gastro-intestinal 


Eye-strain 


Ear  (.otitis) 


Neurasthenia — 
Eye  strain 


"  Spinal  irritation 


Fig.  76. — Reflex  and  symptomatic  head  pains. 

The  accompanying  diagram  shows  some  of  the  relations  of  local- 
ized pain  to  the  cause.  Chronic  occipito-frontal  headaches  are  usually 
neurasthenic,  or  ocular  or  both.  Chronic  occipital  headache  is  usually 
neurasthenic,  ocular  or  uterine. 

Headaches  may  continue  for  a  day  or  may  last  for  weeks  or  months. 
Some  persons  have  headaches  only  when  constipated  or  bilious  or 
when  they  have  an  attack  of  indigestion.  Others  suffer  from  a  little 
pain  nearly  all  the  time,  exacerbations  occurring  at  various  periods. 
Neurasthenic  and  ocular  headaches  are  generally  of  this  type.  When 
headaches  are  persistent,  examination  should  be  made  of  the  eyes  of 
the  nose  and  sinuses;  the  patient  should  be  questioned  as  to  syphilis, 
the  continuous  use  of  tobaccO;  of  tea  and  coffee  and  of  chronic  dyspepsia. 
The  possibility  of  brain  tumor,  of  pachymeningitis  from  blows,  or  sun- 
stroke or  chronic  alcoholism  should  be  considered. 


166  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  persistent  headaches  not  relieved  by  ordinary  treatment  are 
due  to  eye  trouble,  neurasthenia  psychasthenia,  rheumatic  nodules, 
syphilis  or  pachymeningitis.  Eye-strain  may  cause  true  migraine  or 
ordinary  headache.  Eye-strain  headache  is  usually  associated  with  some 
weakness  of  eyesight  and  pains  and  discomfort  about  the  globe,  besides 
severer  pains  at  times  in  the  brow  or  occiput.  The  cause  of  the  eye- 
strain is  usually  astigmatism  and  hypermetropia.  Occasionally  it  is 
due  to  weakness  or  lack  of  balance  of  the  eye-muscles. 

Headaches  may  occur  regularly  every  morning  on  awaking.  They 
are  called  morning  headaches,  and  are  a  symptom  of  neurasthenia,  gastro- 
intestinal toxins  or  arterial  sclerosis.  These  occur  oftenest  in  middle 
life  or  later. 

Symptoms  Associated  with  Headache. — The  symptoms  oftenest 
associated  with  chronic  and  recurrent  headaches  are  vertigo,  somno- 
lence, sensations  of  heat  and  pressure  (cerebral  parsethesias) ,  and  nausea. 
Vertigo  goes  oftenest  with  headaches  of  dyspeptic  origin;  some  of  the  so- 
called  bilious  headaches  of  early  life  develop  later  into  attacks  of  vertigo. 
This  symptom  often  occurs  with  frontal  headaches. 

Pathology. — Headaches  are  to  be  distinguished  from  neuralgias 
and  from  a  special  and  common  form  of  head  pain  known  as  migraine. 

Headaches  are  diffused  pains  caused,  as  a  rule,  by  irritations  lo- 
cated in  or  referred  to  the  peripheral  ends  of  the  fifth  nerve  supplying 
the  dura  mater. 

Neuralgias,  on  the  other  hand,  are  caused  by  irritations  of  the  gang- 
lia or  trunks  of  these  nerves.  The  pains  are  local  and  confined  to  the 
single  branches  of  the  nerve. 

Migraine  is  a  periodical  neurosis  in  which  there  is  a  nervous  dis- 
charge of  force,  not  only  affecting  the  trigeminus,  but  often  other  cranial 
nerves  as  well  as  sympathetic  fibres.  It  is  a  general  disease  of  which 
the  headache  is  only  one  symptom. 

The  nerves  of  the  dura  mater  are  those  most  involved  in  headache. 
Headaches,  when  occipital,  involve  the  sensory  fibres  of  the  vagus 
and  the  upper  four  cervical  nerves.  There  is  no  anatomical  change 
in  the  nerves  except  in  organic  headaches.  But  in  many  cases  the 
membranes  of  the  brain  and  their  sensory  nerves  are  congested  or 
anaemic. 

Diagnosis. — No  symptom  requires  more  careful  investigation  as  to 
its  cause  than  that  of  headache;  for  the  diagnosis  is  always  to  be  made, 
not  of  this  symptom,  but  of  its  cause.  Most  of  the  foregoing  descrip- 
tion accordingly  refers  to  etiology. 

Headaches  which  persist  for  months,  are  worse  in  the  day  and  leave 
the  patient  able  to  sleep  at  night,  to  recur  on  waking,  are  exhaustion 
pains  and  are  due  to  a  neurasthenic  state. 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL   NERVES         167 

Chronic  headaches,  worse  at  night,  are  usually  of  specific  or  organic 
■origin. 

Migrainous  or  "sick-headache"  comes  on  paroxysmally,  lasts  a 
short  time,  and  then  leaves  the  patient  feeling  perfectly  well  or  even 
better  than  ever.  The  attacks  are  often  accompanied  with  nausea, 
flashes  of  light,  strong  pulsations  of  the  head,  vertigo,  pallor  or,  more 
rarely,  congestion  of  the  face. 

In  neuralgic  headaches  the  pains  are  sharp  and  shooting;  they  run 
along  the  tract  of  the  nerve,  and  often  are  associated  with  suffusion 
of  the  eye  and  oedema.     Tender  points  are  felt. 

Most  of  the  persistent,  recurrent  headaches  are  of  migrainous  origin. 

Treatment. — -The  constitutional  treatment  is  based  upon  the  etiology. 
Tonic  measures,  regulation  of  diet,  securing  a  regular  movement  of  the 
bowels,  attention  to  ocular  troubles,  abstention  from  tobacco  and 
alcohol  and  overwork  are  the  important  measures. 

The  symptomatic  treatment  consists  in  giving  sedative  drugs  and 
local  anodynes.  The  coal-tar  products,  antipyrin,  pyramidon,  anti- 
febrin,  are  the  best  symptomatic  remedies. 

Antipyrin  can  be  given  in  doses  of  gr.  v.  every  twenty  minutes 
until  three  or  four  doses  are  taken.  Phenacetin  often  needs  to  be 
given  in  large  doses  of  ten  or  even  twenty  grains.  Antifebrin  must 
be  given  in  small  doses.  Combinations  of  caffeine  citrate  and  the 
various  coal-tar  products  furnish  the  basis  for  the  ordinary  headache 
cures.  Local  applications  of  a  20  per  cent,  solution  of  menthol,  the 
ice  bag,  cloths  wrung  out  in  hot  water  or  a  piece  of  sheet  lint  soaked  in 
chloroform  liniment  two  parts  and  tincture  of  aconite  one  part  are  ef- 
ficacious measures.  A  cathartic,  rest  in  a  darkened  room,  light  diet — ' 
all  these  are  measures  which  many  patients  themselves  learn  to  adopt. 

In  headaches  from  organic  disease,  we  have  to  resort  to  iodide  of 
potassium,  mercury,  arsenic,  salvarsan  and  the  use  of  some  preparation 
of  opium. 

As  will  be  seen,  each  case  of  headache  requires  special  treatment 
and  a  certain  amount  of  experimentation  in  order  to  learn  the  idio- 
syncrasy of  the  patient. 

MIGRAINE  (SICK-HEADACHE,  HEMICRANIA) 

Migraine  is  a  constitutional  neurosis  characterized  by  periodical 
attacks  of  pain  chiefly  in  the  course  of  the  fifth  nerve.  The  pain  is  often 
associated  with  nausea  or  vomiting,  mental  depression,  vasomotor  dis- 
turbances, such  as  flushing,  or  pallor  of  the  face,  by  flashes  of  light,  vertigo, 
tinnitus  aurium,  and  in  rare  cases  by  partial  paralysis  of  one  oculo- 
motor nerve. 


168  DISEASES    OF    THE    NERVOUS    SYSTEM 

It  will  thus  be  seen  that  migraine  is  more  than  ordinary  headache 
and  unlike  an  ordinary  neuralgia. 

Etiology. — The  disease  is  very  common  in  civilized  countries  and  is  fre- 
quent in  America.  It  occurs  oftener  in  women  than  men  in  the  proportion 
of  about  three  to  one,  and  it  begins  in  most  cases  at  or  a  little  before  the 
age  of  puberty.  It  may  begin  as  early  as  the  fifth  or  even  the  second 
year.  It  occurs  in  neurotic  families,  and  there  is  very  often  a  history 
of  direct  inheritance.  Other  neuralgic  troubles,  epilepsy  and  gout  may 
be  found  in  the  family  history.  The  attacks  occur  oftenest  in  the  winter 
in  our  climate.  The  cases  that  begin  in  childhood  and  early  life  are 
sometimes  started  by  overwork  at  school,  but  usually  no  especial  cause 
can  be  found.  When  they  begin  after  maturity,  a  history  of  excesses 
in  work,  injury,  shock  or  exhausting  disease  is  found.  Migrainous 
patients  often  have  some  refractive  disorder  of  the  eye  or  a  weakness  of 
eye-muscles,  and  these  conditions  may  be  factors  in  bringing  on  or  keep- 
ing up  the  headaches.  Endogenous  toxemia  and  especially  poisons  de- 
veloped in  the  intestinal  tract  are  an  important  factor  in  migraine. 

Symptoms. — The  patient  for  several  days  may  feel  a  sense  of  malaise 
and  depression;  usually,  however,  the  prodromal  stage  lasts  only  a  few 
hours  or  a  day.  The  attack  often  comes  on  in  the  morning  and  gradually 
increases  in  intensity  until  the  victim  has  to  give  up  work  and  lie  down. 
Sometimes  the  pain  comes  on  with  almost  epileptic  suddenness  and 
violence,  waking  a  person  from  sleep  or  compelling  him  at  once  to  lie 
down.     Fulgurating  migraine  is  the  term  applied  to  this  type. 

The  pain  starts  in  one  side  of  the  head,  usually  in  the  temple  and  eye, 
but  often  in  the  occiput.  It  increases  and  finally  may  involve  the  whole 
head.  The  pain  is  of  a  tense,  throbbing  character,  increased  by  jars, 
light  and  noises.  It  is  accompanied  sometimes  by  dimness  of  vision, 
often  by  flashes  of  light  or  by  dark  or  light  spots,  variously  colored,  float- 
ing before  the  eyes  (Fig.  77).  Contraction  of  the  visual  field,  usually  in 
the  form  of  bilateral  hemianopsia,  may  occur.  Vertigo,  tinnitus  aurium, 
confusion  of  ideas,  feeling  of  stupor,  disturbances  of  memory,  are  not 
uncommon;  nausea  and  even  vomiting  are  the  rule.  The  vomited  matter 
is  at  first  chiefly  mucus,  but  it  may  later  become  yellow  and  bitter  from 
the  presence  of  bile.  Hence  the  term  "bilious  headache,"  which  is  an 
improper  one,  because  the  bile  is  only  the  result  of  retrostalsic  action 
from  the  vomiting.     Migraine  is  not  the  result  of  gastric  or  liver  disorder. 

The  patient's  face  usually  is  pale  and  gives  the  evidence  of  acute 
suffering.  The  flushed  face  is  very  rare;  the  distinction  between  angio- 
spastic or  pallid  migraine  and  angioparalytic  or  congestive  migraine  is 
not  of  clinical  value.  The  blood  pressure  may  rise  and  the  pulse  be 
lessened  in  rapidity.     The  temperature  in  children  often  rises. 

The  attack  lasts  from  six  to  twelve  or  twenty-four  hours,  occasionally 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES 


169 


even  two  or  three  days.  As  the  intensity  of  the  pain  lessens,  the  patient 
sinks  to  sleep,  and  awakens  next  morning  feeling  lefreshed  and  better 
than  before  the  attack. 

The  attacks  occur  at  varying  periods,  fortnightly  or  monthly,  and 
even  weekly.  In  women  they  often  occur  during  menstruation.  Some 
women  are  entirely  free  from  them  during  pregnane}'-.  At  about  the 
time  of  the  menopause  in  women,  and  at  about  the  same  time  of  life  in 


Fig.  77. — Scintillating   and   zig-zag   lights   seen   in   migraine.      (Babinski.) 

men,  the  disease  lessens  in  severity  and,  as  a  rule,  disappears.  Some  form 
of  neuralgia  or  some  neurosis  in  rare  cases  takes  its  place. 

Complicating  Symptoms. — Partial  oculomotor  paralysis,  temporary 
aphasia,  slight  hemiplegia,  heminumbness,  pecuhar  odors  or  tastes, 
convulsive  movements  of  the  body  almost  resembling  epileptic  attacks 
occur. 

Cases  presenting  these  symptoms  are  rare.  When  they  occur  in 
one  case,  however,  they  usually  occur  in  each  attack  unless  it  is  modified 
by  treatment. 


170  ■  DISEASES    OF   THE    NERVOUS   SYSTEM 

Vicarious  Attacks. — Migraine  is  sometimes  associated  with  epilepsy 
or  insanity;  that  is  to  say,  persons  in  early  life  have  had  migraine  and 
later  developed  the  diseases  mentioned.  The  relation  between  these 
diseases,  is  not,  however,  a  very  close  one,  nor  does  one  disease  lead  to 
the  other.  The  attack  of  migraine  is  sometimes  replaced  by  various  other 
functional  neuroses.  Sometimes,  instead  of  a  fully  developed  attack, 
the  patient  has  a  sense  of  mental  depression,  with  confusion  of  ideas. 
Cases  have  been  reported  in  which  acute  mania  took  the  place  of  the 
headache. 

Types. — Practically,  we  find  two  classes  of  cases: 

1.  The  typical,  associated  with  visual  disorders  and  having  most 
of  the  symptoms  described  above. 

2.  The  irregular  or  mixed  type,  in  which,  with  many  symptoms  of 
ordinary  migraine,  there  is  a  history  of  rheumatic  influences  and  often 
of  anaemia  or  dyspepsia.  These  are  cases  of  a  true  migrainous  affection 
complicated  with  some  form  of  symptomatic  headache,  such  as  has  been 
already  described.  The  mixed  or  irregular  migraines  are  important 
to  recognize,  for  they  call  for  special  treatment.  Many  patients  have 
their  ''sick-headaches"  and  their  "neuralgic  headaches,"  so-called,  and 
they  distinguish  between  them.  Both  are  migrainous  headaches,  but 
with  other  elements  entering. 

Pathology. — The  seat  of  the  pain  is  chiefly  in  the  intracranial  branches 
of  the  fifth  nerve  and  of  the  pneumogastric;  the  upper  cervical  nerves, 
however,  are  often  involved.  There  are  no  morbid  anatomical  changes 
known.  The  most  plausible  theory  of  the  disease  is  that  it  is  a  fulgurat- 
ing neurosis,  in  which  there  are  periodical  discharges  of  nerve  force,  or 
nerve  storms.  The  seat  of  the  discharge  is  perhaps  in  the  cerebral 
cortex,  or  possibly  in  the  primary  sensory  centres,  i.e.,  the  root  ganglia 
of  the  fifth  and  vagus  nerves.  The  disease  is  certainly  not  in  the  sympa- 
thetic system,  as  was  once  taught.  The  presence  of  excess  of  some 
endogenous  poison  as  a  factor  in  the  disease  may  be  regarded  as  most 
probable. 

Diagnosis. — The  diagnosis  is  based  upon  the  hereditary  history,  the 
periodicity  and  seat  of  the  attacks,  the  nausea,  the  complicating  visual 
and  other  sensory  symptoms.  It  should  not  be  forgotten  that  the  same 
patient  may  have  migraine  and  other  neuralgias  or  may  have  also  an 
organic  brain  or  renal  disease. 

Treatment — Prophylaxis. — Children  of  families  in  which  this  neurosis 
exists  should  be  carefully  watched  during  the  ages  between  five  and 
twenty.  The  eyes  and  nose  should  be  examined.  They  should  not  be 
subjected  to  excessive  mental  or  visual  strain,  and  if  attacks  develop  they 
should  be  promptly  treated.  The  application  of  glasses  should  be  con- 
sidered, but  not  hastily  adopted. 


SENSORY    NEUROSES    OF   THE    CEREBROSPINAL    NERVES         171 

As  regards  constitutional  treatment,  the  best  measures  for  curing  a 
case  of  migraine  consist  in  correcting  any  visual  or  nasal  defect,  and  pre- 
scribing such  diet  and  exercise  as  secure  health  to  the  body  and  the 
nerves.  Often  a  rest-cure  or  half-rest-cure  is  absolutely  needed.  The 
diet  should  be  very  simple  and  non-fermentative.  It  should  be  mainly  of 
meat,  fish,  green  vegetables  and  cooked  fruits.  The  meats  should  be  mod- 
erate in  amount,  and  sometimes  only  fish  and  poultry  should  be  allowed. 

Of  the  drugs,  alkaline  tonics,  given  well  diluted  before  meals,  are  the 
most  trustworthy.  Extract  of  cannabis  indica  may  be  given  in  large  doses 
and  for  a  long  time  (gr.  3^^  to  gr.  i.,  ter  in  die).  The  salicylates  are  useful 
combined  with  an  alkaline  laxative  like  Rochelle  salts,  a  dose  being  taken 
night  and  morning.  Much  stress  is  laid  by  some  upon  ocular  muscular 
insufficiencies,  and  I  believe  that  such  conditions  should  be  remedied,  but 
place  little  confidence  in  them  alone.  On  the  other  hand,  the  correction 
of  small  or  large  degrees  of  astigmatism  and  hypermetropia  sometimes 
produces  suprisingly  good  results.  The  reported  cure  of  numerous  cases 
of  migraine  by  treatment  of  nasal  hypertrophies  and  catarrh  should  not 
excite  too  much  confidence  in  such  measures.  In  fact,  since  migraine  is  a 
constitutional  neurosis,  one  cannot  expect  permanent  results  from 
removing  reflex  irritants  alone. 

For  the  relief  of  the  attack  the  measures  recommended  under  headache 
are  to  be  used.  All  drugs  lose  their  effect  after  a  time,  and  finally 
patients  give  up  treatment  or  resort  to  codein  or  morphine.  Chloral  and 
a  hot  foot-bath  break  up  attacks  sometimes.  Locally  galvanic  currents 
are  sometimes  helpful,  and  so  are  static  sparks.  Hot  applications  and 
pencilling  with  menthol  give  relief  to  some.  Quiet  and  rest  are  spon- 
taneously resorted  to. 

NEUROSES  OF  THE  SENSORY  BRANCH  OF  THE  SEVENTH  NERVE 

As  stated  under  the  head  of  Facial  Palsy,  the  seventh  nerve  has  a 
sensory  part,  and  its  disorders  cause  otalgia  of  simple  type,  an  ''otalgic 
tic  douloureux"  and  a  herpetic  otalgia,  due  to  lesion  of  the  geniculate 
ganglion.  When  both  motor  and  sensory  fibres  are  involved,  there 
results  the'' Hunt  syndrome"  of  facial  palsy,  otalgia  and  herpes  of  the  ear, 

NEUROSES  OF  THE  ACOUSTIC  NERVE 

Anatomy. — The  auditory  or  eighth  cranial  nerve  has  two  different  parts.  One 
portion  passes  to  the  cochlea  and  utricle  and  saccules;  it  has  to  do  with  the  sense  of 
hearing;  the  other  goes  to  the  semicircular  canals,  and  has  to  do  with  that  sense  by 
which  we  appreciate  the  position  of  our  body  and  its  relations  to  space.  The  eighth 
nerve  is  thus  an  auditory  and  a  space-sense  nerve. 

The  acoustic  fibres  enter  the  medulla  by  two  roots,  a  lateral  and  a  median.  The 
lateral  root  has  mainly  auditory  fibres.     The  space-sense  fibres  enter  chiefly  by  the 


172  DISEASES    OF    THE    NERVOUS    SYSTEM 

median  root.  These  roots  are  connected  with  three  nuclei,  viz. :  (1)  The  chief  nucleus, 
(2)  Deiter's  nucleus  and  (3)  the  accessory  nucleus. 

The  lateral  root  is  the  one  coming  from  the  cochlea,  and  is,  as  stated,  mainlj^  a  nerve 
of  hearing. 

The  median  root  is  connected  chiefly  with  Deiter's  nucleus  (2)  and  through  this 
with  the  longitudinal  bundle  and  with  the  vestibulo-spinal  tract  and  anterior  horns  of 
the  cord.     Fibres  also  go  to  the  vermis. 

The  disease  of  the  eighth  or  acoustic  and  space-sense  nerve  which  are  of  special 
interest  to  the  neurologists  are  auditory  paralysis  or  nervous  deafness,  hyperacusis, 
tinnitus  aurium,  and  auditory  vertigo,  or  Meniere's  disease.  These  diseases  correspond 
with  loss,  excess  and  perversion  or  irritation  of  function. 

NERVOUS  DEAFNESS  (ACOUSTIC  PARALYSIS) 

Nervous  deafness  may  be  due  to  lesions  (1)  of  the  two  cortical  centres 
of  hearing,  (2)  of  the  acoustic  nuclei,  and  (3)  of  the  acoustic  nerve  itself 
or  its  end  organ ;  (4)  it  may  be  psychogenous  or  hysterical.  Practically, 
it  is  almost  always  the  nerve  and  the  internal  ear  which  are  affected. 

Etiology. — 1.  Cortical  nervous  deafness  has  been  known  to  occur  in  a 
few  instances  from  lesions  of  both  temporal  lobes  (Mills,  Mott).  The 
deafness  of  hysteria  is  of  cortical  (psychic)  origin. 

2.  Deafness  from  lesion  of  the  acoustic  nucleus  or  nerve-root.  Cere- 
brospinal meningitis  in  the  young  and  syphilitic  meningitis  in  the  adult 
are  the  more  frequent  causes  of  this  form.  Fractures,  tumors  and 
hemorrhages  may  also  be  causes.  When  the  auditory  nucleus  and  nerve- 
root  are  affected  by  these  diseases,  its  peripheral  terminations  in  the 
labyrinth  are  also  often  involved,  so  that  sharp  distinction  cannot  always 
be  drawn  between  this  form  and  that  due  to  labyrinthine  disease. 

3.  Deafness  from  Labyrinthine  Disease. — The  causes  are  drugs,  such 
as  quinine  and  the  salicylates;  inflammations,  including  syphilitic  exu- 
dates; injuries;  hemorrhages;  tumors;  primary  atrophy,  which  may  be 
of  family  or  hereditary  type;  and  may  occur  in  locomotor  ataxia; 
mechanical  causes,  such  as  the  constant  noises  and  jarring  to  which 
locomotive  engineers  and  boiler-makers  are  subject. 

4.  Hysterical  deafness  is  caused  by  some  morbid  mental  state  or 
subconscious  complex. 

Symptoms  of  Nervous  Deafness. — The  dominant  symptom  is  loss  of 
hearing,  but  this  may  be  accompanied  by  vertigo,  tinnitus  and  even  forced 
movements. 

In  hysterical  or  psychogenous  deafness  the  loss  of  hearing  is  rarely 
complete,  is  usually  unilateral,  is  more  a  bone  conduction  deafness  and 
especially  involves  high  and  low  notes.  It  is  usually  temporary.  I 
have  seen  cases,  however,  where  these  characteristics  were  absent. 

Deafness  from  involvement  of  the  nucleus  and  nerve-root  is  usually 
accompanied  by  symptoms  of  a  basilar  meningitis  or  lesion  of  the  pons 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         173 

and  medulla.  Labyrinthine  deafness  is  often  associated  with  vertigo, 
tinnitus  and  forced  movements,  when  it  may  ))ecome  a  symptom-com- 
plex known  as  "Meniere's  disease." 

Sudden  total  deafness  is  characteristic  of  hysteria  and  of  syphilitic 
disease  of  the  internal  ear.  In  genuine  nervous  deafness,  unless  the 
deafness  is  absolute,  hearing  by  bone  conduction  is  lost  or  lessened, 
while  aerial  conduction  is  preserved.  A  tuning-fork  vibrating  on  mas- 
toid is  not  heard  by  the  affected  ear,  though  it  is  heard  when  held  in 
the  air  close  by  this  ear.     (Rinne's  test). 

Normally  a  vibrating  tuning  fork  with  its  base  placed  on  the  vertex 
of  the  skull  is  heard  in  both  ears.  If  there  is  disease  of  the  conducting 
apparatus  it  seems  to  the  patient  that  he  hears  the  fork  in  the  ear  of  the 
affected  side.  This  is  called  a  ''Positive  Weber."  In  cases  of  disease 
of  the  auditory  nerve,  the  sound  of  the  fork  will  seem  to  ))e  heard  on 
the  sound  side.     This  is  the  "Negative  Weber." 

TINNITUS  AURIUM.     TINNITUS  CEREBRI  (NOISES  IN  THE  EAR  AND  HEAD) 

Subjective  sounds  resembling  hissing,  buzzing,  humming,  beat- 
ing, muscial  notes,  etc.,  are  classed  together  under  the  general  head  of 
tinnitus  aurium.     It  is  a  very  common  symptom. 

Etiology. — The  disease  attacks  adults  in  middle  and  later  life.  Men 
and  women  are  alike  affected.  Persons  of  neuropathic  constitution  and 
high,  blood  pressure  are  more  susceptible  to  the  trouble.  The  arterio- 
sclerosis of  old  age,  cerebral  congestion,  sunstroke,  tobacco  and  alcoholism 
predispose  to  it.  It  occurs  often  in  involutional  melancholia  and  in 
neurasthenia.  Some  local  disease  or  congestion  of  the  middle  or  internal 
ear  is  usually  present. 

Disease  of  the  auditory  nuclei  and  auditory  tracts  rarely,  if  ever, 
causes  tinnitus;  but  chronic  pachymeningitis,  such  as  follows  blows 
on  the  head,  sunstroke,  alcoholism,  etc.,  may  be  attended  by  most 
annoying  tinnitus,  which  is  often  not  so  much  in  the  ears  as  in  the 
head — a  tinnitus  cerebri.  In  old  people  with  thickened  arteries  and 
imperfect  brain  nutrition  a  similar  condition  may  occur. 

Tinnitus  accompanies  confusional  psychoses  sometimes,  and  may  be 
the  source  of  aural  hallucinations. 

A  kind  of  tinnitus  may  accompany  migraine  and  it  may  take  the 
form  of  an  aura  in  epilepsy. 

Despite  this  long  list  of  causes,  the  chief  factors  may  be  summed 
up  as  neurasthenic  states,  local  ear  disease,  humoral  poisons  and  irri- 
tants and  arteriosclerosis. 

The  syrn-ptoms  are  indicated  by  the  name  of  the  malady.  They  may 
come  on  suddenly,   but  usually  develop  slowly.     Some  deafness  and 


174  DISEASES    or   THE    NERVOUS    SYSTEM 

occasional  vertigo  are  often  present.  The  noise  is  located  in  one  ear, 
as  a  rule.  Sometimes  it  is  said  to  be  simply  "in  the  head."  The 
sounds  are  generally  present  all  the  time,  giving  the  patient  little  rest 
and  making  life  a  burden.  They  vary  greatly  in  character  and  in- 
tensity.    These  variations  are  indicated  in  the  study  of  the  diagnosis. 

The  Diagnosis. — The  recognition  of  the  symptom  is  easy.  The 
principal  thing  is  to  discover  its  seat  and  cause. 

The  ear  should,  of  course,  be  examined  for  external  or  middle-ear 
disease. 

If  the  tinnitus  is  pulsating  and  synchronous  with  the  heartbeats 
and  stopped  by  carotid  compression,  it  may  be  inferred  that  it  is  due  to 
vasomotor  paralysis  or  inflammatory  congestion  or  aneurism. 

If  the  sound  is  not  in  the  ear,  but  in  the  head,  and  not  associated 
with  deafness  or  ear  disease,  the  trouble  is  probably  central,  and  most 
likely  is  of  meningeal  or  arteriosclerotic  origin. 

Noises  which  are  complex  or  take  the  form  of  musical  sounds  or 
words  are  probably  central  and  illusional. 

Constant  rushing,  knocking,  pulsating  noises  are  due  to  conges- 
tion, hemorrhage  or  inflammatory  effusion  in  the  labyrinth. 

Moist  sounds  of  a  gurgling,  bubbling,  boiling,  singing,  whistling, 
shell-like  roaring  character  indicate  disease  of  the  middle  ear,  with 
fluid  exudation,  catarrh  of  the  Eustachian  tube,  or  irritation  of  the 
external  auditory  canal  or  mastoid  cells. 

Dry  roaring  and  ringing  noises  are  due  to  non-suppurative  catarrh 
of  the  middle  ear,  disease  of  the  muscles  or  nervous  supply  of  the 
tympanum. 

The  condition  of  the  digestion  should  be  inquired  into  and  the  ex- 
istence of  renal,  arterial  or  central  nervous  disease  investigated. 

Treatment. — Ear  disease  must  be  treated  if  it  is  present.  Hydro- 
bromic  acid  and  the  other  bromides,  given  in  ordinary  doses,  are  the 
surest  palliating  measures  for  this  trouble.  They  may  be  combined 
with  digitalis.  Iodide  of  potassium  and  iodide  of  ethyl  often  are  useful. 
Nitroglycerin  is  sometimes  of  value  in  patients  with  hard  arteries.  A  com- 
bination of  digitalis,  bromide,  and  nitroglycerin  has  given  very  good  results. 
Often  general  tonic  measures  are  needed,  and  often  also  the  patient  must 
be  taught  to  be  patient  with  an  ailment  that  cannot  be  cured. 

VESTIBULAR  NEUROSES  (VERTIGO,  DIZZINESS,  GIDDINESS) 

The  vestibular  nerve  has  to  do  with  our  sense  of  equilibrium,  oculo- 
motor control,  orientation  of  the  body  and  extremities.  When  it  is 
disordered  we  get  the  symptoms  of  vertigo — staggering,  nystagmus,  nausea, 
and  loss  of  power  correctly  to  orient  the  extremities.  To  determine 
the  condition  of  the  vestibular  nerve  there  are  certain  tests  made. 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         175 

The  Bar  any  Tests.- — The  vestibular  nerve  has  its  central  connections 
with  three  ganglia  in  the  medulla  and  from  these  ganglia  it  sends  connect- 
ing fibres  to  the  vermis  of  the  cerebellum,  to  the  posterior  longitudinal 
bundle,  probably  fibres  to  the  red  nucleus  and  the  cerebral  cortex  and 
via  Deiter's  nucleus  to  the  motor  cells  of  the  spinal  cord. 

When  this  nerve  is  irritated,  it  produces  the  symptoms  of  dizziness, 
nystagmus,  inco-ordination  and  disorientation. 

The  Barany  test  is  one  which  enables  one  to  determine  whether  the 
nerve  is  intact  and  can  send  its  impulses  through  to  its  normal  desti- 
nation. The  test  in  all  its  details  is  quite  elaborate,  but  it  is  sufficient  for 
ordinary  routine  neurological  examination  to  use  simply  the  cold  water 
method. 

The  patient  sits  in  a  chair  and  the  examiner  injects  half  a  dozen  two- 
ounce  syringefuls  of  cold  water  into  the  external  meatus.  The  operator 
should  be  careful  to  have  the  water  strike  the  side  of  the  meatus  and  not 
be  sent  with  any  force  against  the  membrane. 

After  this  operation,  if  the  vestibular  reflex  is  normal  the  patient  will 
feel  dizzy  and  stagger,  there  will  be  a  lateral  nystagmus  away  from  the 
ear  which  has  been  irritated  and  his  finger  will  "pass  the  point,"  e.g.:  if 
the  patient  is  told  to  place  the  finger  of  his  outstretched  hand  upon  the 
finger  of  the  examiner,  shut  his  eyes,  raise  the  hand  to  a  vertical  position 
and  bring  it  down  so  as  to  touch  the  examiner's  finger  again,  he  will  miss 
the  finger  and  it  will  pass  several  inches  to  one  side.  If  the  hand  of  the 
patient  is  dropped  to  the  side  and  the  same  test  made,  or  if  the  arm  is 
carried  out  horizontally  at  right  angles  to  the  examiner's  finger,  he  will 
also  "pass  the  point."  If  there  is  complete  blocking  of  the  nerve 
and  the  labyrinth  is  "dead"  there  will  be  no  nystagmus,  or  vertigo 
or  passing  of  the  point.  If  there  is  no  nystagmus  it  may  be  inferred 
that  the  connections  of  the  nerve  with  the  longitudinal  bundle  are 
affected. 

The  test  is  also  made  by  using  hot  water,  by  the  galvanic  current  and 
by  rotating  the  patient  while  sitting  on  a  stool. 

Vertigo  is  a  disturbance  of  consciousness  characterized  by  apparent 
movements  of  external  objects  or  of  the  person  himself.  If  external 
objects  whirl  around,  the  vertigo  is  called  objective;  if  the  person  himself 
seems  to  move,  it  is  called  subjective.  Vertigo  is  almost  always  a  symp- 
tom. In  rare  cases  it  appears  to  be  essential,  i.e.,  due  to  a  functional 
nerve  discharge  like  the  aura  of  epilepsy. 

Vertigo  is  connected  more  or  less  with  our  space  sensations,  and 
hence  it  comes  under  disorders  of  the  vestibular  branch  of  the  eighth 
cranial  nerve  and  its  central  representations. 

Etiology. — The  causes  of  vertigo  may  be  classed  somewhat  like  those 
of  headache,  as  follows: 


176  DISEASES    OF    THE    NERVOUS    SYSTEM 

(1)  Hsemic,  etc.,  anaemia,  hypersemia,  gastro-intestinal  and  other 
endogenous  toxins;  toxaemia  from  tobacco  and  alcohol;  (2)  arteriosclerosis, 
(3)  vestibular  nerve  irritation;  (4)  neuroses:  epilepsy,  neurasthenia;  (5) 
reflex:  ocular,  gastric;  (6)  organic  brain  disease;  (7)  mechanical  causes, 
like  electricity,  swinging,  etc. 

Based  mainly  on  the  etiology,  we  have  as  a  practical  classification  of 
ordinary  cases  of  vertigo:  autotoxic,  arterio-sclerotic,  vestibular,  ocular 
and  neuropathic  forms.  The  various  causes  of  vertigo  act  by  irritating 
the  space-sense  nerve  and  thus  disturbing  our  sense  of  relation  to  external 
objects,  and  by  irritating  cortical  centres.  Vertigo  is  a  painful  response 
of  the  vestibular  nerve  as  neuralgia  is  a  painful  response  of  the  fifth 
nerve.  Vertigo  may  be  due  to  organic  lesions  of  the  cerebellum  and 
its  peduncles;  it  is  then  associated  with  forced  movements  of  the 
body. 

Symptoms. — Vertigo  comes  on  suddenly,  and  lasts,  as  a  rule,  for  but 
a  moment.  The  floor  rises  and  sinks,  or  objects  whirl  around  (objective 
vertigo),  or  the  patient  seems  whirling  around  or  falling.  The  ideas  are 
confused;  there  are  a  sense  of  alarm  and  a  feeling  of  faintness.  The 
patient  totters,  sometimes  falls;  there  may  be  nausea  or  vomiting.  In 
some  forms  there  is  momentary  loss  of  consciousness  or  syncope.  Vertigo 
usually  comes  on  in  short  attacks,  but  in  toxsemic  states,  as  in  alcoholism 
or  nicotinism,  it  is  almost  constant  while  the  poison  is  in  the  system. 
Vertigo  may  become  chronic  or  nearly  so;  and  if  severe  it  forms  what  is 
called  the  status  vertiginosus  (Mitchell).  Vertigo  is  increased  by  rising 
or  sudden  movements  and  lessened  by  lying  down. 

Symptoms  of  Special  Forms — Auditory  Vertigo  {Meniere's  Disease). — 
A  large  proportion  of  severe  periodical  vertigoes  are  due  to  disease 
or  irritation  of  the  eighth  nerve  and  its  centres.  The  common  cause  is 
local  disease  of  the  labyrinth.  When  this  produces  severe  attacks  of 
vertigo  with  nausea  and  perhaps  syncope,  it  is  called  "Meniere's  disease." 
The  name  is  often  applied  to  any  form  of  auditory  vertigo.  Meniere's 
type  is  always  due  to  organic  disease  of  the  labyrinth.  It  is  usually 
accompanied  by  progressive  deafness,  and  sometimes  by  tinnitus  and 
forced  movements  or  even  utter  inability  to  walk  steadily.  When  the 
deafness  is  complete  the  vertigo  ceases,  because  the  nerve  end-organ  is 
destroyed.  Mild  forms  of  auditory  vertigo  present  nothing  unusual 
except  those  due  to  involvement  of  the  nerve  of  hearing. 

Bilious  and  Stomachal  Vertigo. — In  condition  of  dyspepsia,  consti- 
pation and  hepatic  torpor,  the  loaded  and  disordered  stomach  and  bowel 
suddenly  discharge  into  the  blood  irritant  substances  which  pass  to  the 
brain  and  by  direct  action  on  the  nervous  centres  cause  vertigo.  This 
is  probably  the  explanation  of  the  vertigo  of  biliousness  and  constipation. 
It  is  a  paroxysmal  vertigo,  noted  most  in  the  morning,  not  very  severe. 


SENSORY    NEUROSES    OF   THE    CEREBROSPINAL    NERVES         177 

and  often  accompanied  by  nausea.  Stomachal  vertigo  is  more  acute, 
severe  and  may  be  accompanied  with  loss  of  consciousness. 

Neuro-pathic  Vertigo. — ^The  symptoms  of  epileptic  vertigo  will  be 
described  under  that  head. 

Neurasthenic  vertigo  is  a  not  uncommon  symptom.  The  attacks 
are  short,  generally  subjective,  not  severe  or  accompanied  by  nausea  or 
syncope,  but  they  often  cause  much  alarm.  Underlying  them  are  ex- 
hausted and  irritable  nerve-centres,  with  ocular,  gastric  and  humoral 
irritations  or  a  weak  heart. 

A  neuropathic  vertigo  occurs  sometimes  in  the  form  of  attacks  almost 
exactly  resembling  seasickness.  There  are  intense  vertigo,  nausea, 
and  faintness  lasting  for  hours,  coming  on  suddenly  without  known  cause 
except  overwork  or  excitement.  The  attacks  occur  in  neurotic  subjects 
and  are  analogous  to  the  other  nervous  crises.  It  is  a  periodical  neurosis 
of  the  space-sense  nerve  and  resembles  migraine. 

A  form  of  vertigo  which  is  'psychical  in  character  occurs  in  neuras- 
thenics. It  consists  in  a  sudden  sensation  of  insecurity,  an  apprehension 
of  falling,  of  an  approaching  loss  of  consciousness.  There  is  no  true 
vertigo,  either  subjective  or  objective,  and  the  patients  really  never  stagger 
or  fall.     It  is  a  psychosis  rather  than  a  nervous  condition. 

In  some  nervous  subjects  there  occurs  a  sudden  giving  way  of  the 
legs.  There  is  no  conscious  vertigo,  yet  such  probably  exists.  The 
symptom  is  noted  in  exophthalmic  goitre,  paralysis  agitans  and  epilepsy. 

Ocular  vertigo  is  a  rare  symptom,  but  is,  when  present,  chronic  and 
annoying.  It  is  caused  by  refractive  errors  and  unequal  action  of  the 
ocular  muscles. 

The  mechanical  vertigoes,  such  as  seasickness,  car  sickness,  etc.,  are 
produced  by  swinging  or  whirling,  the  movements  of  the  ship,  steam 
car  and  elevators.  Railway  mail  clerks,  elevator  boys,  often  suffer 
from  chronic  disturbances  of  a  vertiginous  character.  Ocular  and 
auditory  nerve  sensations  enter  mainly  into  the  causation  of  the 
troubles. 

Arteriosclerotic  Vertigo,  Senile  Vertigo. — This  occurs  in  persons 
who  have  arteriosclerotic  changes  in  the  brain  or  labyrinth  vessels,  either 
from  disease  or  senility.  The  symptom  is  caused  by  impaired  brain 
nutrition  with  consequent  ansemia.  Senile  vertigo  may  also  be  due  to  a 
weak  and  fatty  heart. 

Diagnosis. — In  investigating  vertigo  the  physician  should  find  (1) 
whether  it  is  subjective  or  objective;  (2)  paroxysmal  or  chronic;  (3) 
accompanied  by  ear  symptoms,  nausea,  tinnitus,  and  loss  of  consciousness. 
He  should  then  direct  himself  to  finding  the  special  cause  and  seat, 
remembering  that  the  vestibular,  gastric,  toxic,  and  neurasthenic  are  the 
common   forms.     In   elderly   persons   the   arteries  should  be  carefully 

12 


178  DISEASES    OF    THE    NEEVOUS    SYSTEM 

examined.  In  young  persons  the  possibility  of  epilepsy  must  be 
remembered. 

The  prognosis  depends  upon  the  cause.  Epileptic  vertigo  and  vertigo 
from  organic  disease  are  most  serious.  Meniere's  vertigo  usually  ceases 
when  complete  deafness  occurs.  The  other  forms  of  vertigo  are  ordinarily 
susceptible  of  relief. 

Treatment. — The  attack  is  treated  by  rest  in  the  horizontal  position 
and  the  administration  of  a  volatile  stimulant.  The  disorder  must  then 
be  treated  in  accordance  with  the  cause. 

In  Meniere's  vertigo  the  use  of  quinine  by  Charcot's  method  is  said 
to  be  useful.  Quinine  is  given  in  doses  which  are  gradually  increased 
until  slight  cinchonism  results;  then  the  drug  is  stopped.  Mitchell 
advises  the  addition  of  hydrobromic  acid;  Gowers  advises  the  use  of 
salicylate  of  sodium  in  five-grain  doses  instead  of  quinine.  Hirt  recom- 
mends ten  drops  of  a  2  per  cent,  solution  of  pilocarpin  injected  hypo- 
dermically  every  other  day.  A  better  method  is  to  give  a  sweating  dose 
of  pilocarpin  muriate,  gr.  Ya.  to  Ho)  with  a  tumbler  of  hot  water  early  in 
the  morning  before  the  patient  rises. 

Neurasthenic  vertigo  is  cured  by  rest  and  attention  to  diet,  laxatives 
and  mineral  acids  being  used.  Hydrobromic  acid  with  pepsin  and 
glycerin  are  often  very  helpful  here.  Gastric  vertigo  is  to  be  treated 
with  saline  laxatives  and  simple  bitters  before  meals. 

In  the  vertigo  of  "biliousness"  and  constipation  there  is  often  a  neu- 
rasthenic element,  and  a  similar  attention  to  diet  and  to  the  digestive 
organs  is  indicated.  In  arteriosclerotic  and  senile  vertigo  small  doses 
of  nitroglycerin  and  iodide  of  potassium,  with  or  without  digitalis, 
should  be  given.  Rest  and  warmth  of  the  extremities  are  indicated. 
In  all  forms  of  vertigo  bromide  of  potassium  is  helpful  and  will  relieve 
the  symptoms  for  a  time.     It  is  the  best  symptomatic  remedy. 

There  are  two  peculiar  forms  of  disease  to  which  the  name  vertigo 
has  been  attached  which  may  be  described  here. 

Laryngeal  Syncope  [Laryngeal  Vertigo,  L.  Epilepsy). — This  is  a  rare  form  of  dis- 
order characterized  by  attacks  of  parsesthesia  of  the  throat,  with  coughing,  followed 
by  sudden  syncope,  and  sometimes  by  slight  convulsive  movements. 

At  the  onset  of  the  attacks  a  burning  or  tickling  sensation  is  felt  in  the  larynx 
or  trachea;  there  is  a  spasmodic  cough,  perhaps  some  asthmatic  or  dyspnoeic  symp- 
toms, when  the  patient  suddenly  falls  unconscious  for  a  short  time.  The  attacks 
may  occur  daily  or  only  once  in  a  few  weeks.  The  disease  is  an  epileptic  or  tabetic 
phenomenon,  or  due  to  local  disease. 

The  treatment  should  be  directed  to  relieving  the  cause. 

Paralyzing  Vertigo  (Gerlier's  Disease). — This  is  a  disease  occurring  only  on  the 
farms  in  southern  France  and  Switzerland. 

The  symptoms  consist  of  sudden  attacks  of  ptosis,  vertigo,  paresis  of  arms  and 
legs  and  cervico-occipital  pain.     The  disease  is  most  prevalent  in  the  summer  time. 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         179 

It  attacks  chiefly  males.  Single  attacks  last  not  over  ten  minutes,  but  may  occur 
frequently. 

The  cause  is  supposed  to  be  a  special  microbe  developed  in  the  stables  during  the 
heat  of  summer. 

We  are  not  aware  of  its  occurrence  in  America,  though  Seguin  called  attention  to 
the  close  similarity  of  the  symptoms  to  those  of  poisoning  by  conium  maculatum. 

SENSORY  NEUROSES  OF  THE  GLOSSOPHARYNGEAL  NERVE 

The  anatomy  of  this  mixed  nerve  is  described  under  the  head  of 
motor  neuroses.  The  sensory  fibres  may  be  affected  in  hysteria,  causing 
the  symptom  called  globus,  and  also  the  pharyngeal  anaesthesia  found  in 
the  same  disease. 

The  special  fibres  of  taste  may  be  affected,  causing  ageusia  or  loss  of 
taste. 

Ageusia  (loss  of  the  sense  of  taste)  is  an  affection  in  which  the  power 
to  discriminate  the  tastes  of  bitter,  sweet,  salt,  acid  and  alkaline  sub- 
stances is  lost. 

Etiology. — Hysteria  may  cause  a  hemiageusia.  Lesions  of  the  corda 
tympani,  of  the  third  root  of  the  trigeminus  or  of  the  glossopharyngeal 
nerve  may  cause  more  or  less  ageusia.  Catarrhal  diseases  of  the  mucous 
membrane  of  the  mouth  and  nose  are  frequent  causes.  It  is  not  caused 
by  cortical  brain  disease  so  far  as  known.  Some  ageusia  is  present 
in  the  imbecile,  and  the  sense  of  taste  is  less  keen  in  the  lowly  organ- 
ized and  criminal  classes. 

Symptoms. — The  symptoms  are  subjective  and  may  not  be  noticed  at 
first  by  the  patient.  In  hemiageusia  from  facial  palsy  and  in  hysteria 
it  has  to  be  looked  for,  as  the  patient  does  not  complain.  The  tests 
are  made  with  solutions  of  salt,  sugar,  vinegar,  and  quinine.  A  single 
solution  of  sugar  usually  answers.  But  the  different  parts  of  the  tongue 
differ  in  sensibility  to  different  substances.  Care  must  be  taken  to 
exclude  the  nose  as  a  factor  in  taste. 

Disease  of  the  trigeminus  and  facial  usually  causes  ageusia  on  the 
anterior  two-thirds  of  the  tongue,  with  loss  of  taste,  especially  for  sour 
and  bitter  substances.  Sometimes,  however,  disease  of  the  trigeminus 
or  disease  of  the  tympanum  involving  the  tympanic  plexus  and  chorda 
tympani  causes  ageusia  of  the  whole  tongue  on  the  affected  side. 

Ageusia  from  disease  of  the  glossopharyngeal  alone  is  very  rare, 
there  is  loss  of  taste  on  the  posterior  third  of  the  tongue,  soft  palate  and 
pillars  of  the  fauces,  to  sweets  and  acids.  A  few  cases  have  been  re- 
ported in  which  paralysis  of  the  glossopharyngeal  caused  complete 
ageusia  on  the  affected  side.  It  must  be  inferred,  therefore,  that  taste 
fibres  run  sometimes  wholly  in  the  fifth,  more  rarely  wholly  in  the  ninth 
nerves,  and  usually  in  both. 


180  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  treatment  depends  on  the  cause.  Locally,  cleansing  and  stimulat- 
ing mouth-washes  and  electricity  may  be  used. 

Parageusia,  or  perversions  and  imperfections  in  the  taste  sense,  are 
very  frequent.  Thej^  are  generally  clue  to  irritation  of  the  taste  nerves 
from  catarrhal  inflammation  of  the  stomach  or  mouth.  They  also  occur 
in  hysteria  and  in  syphilis. 

SENSORY  NEUROSES  OF  THE  UPPER  CERVICAL  NERVES 

The  mass  of  muscles  at  the  back  of  the  neck  is  made  up  of  nine  in- 
d'vidual  muscles  on  each  side.  They  are  innervated  by  the  posterior 
branches  of  the  upper  six  cervical  nerves  and  the  spinal  accessory. 

Sensation  is  supplied  to  this  muscular  mass  and  to  the  back  of  the 
head  and  neck  by  the  anterior  branches  of  the  second,  third  and  fourth 
cervical  and  the  posterior  branches  of  the  second  cervical.  The  cuta- 
neous distribution  of  these  nerves  is  shown  in  the  diagrams.  (Figs.  27 
and  28.) 

From  a  study  of  the  innervation  of  the  skin  and  muscles  of  the  neck, 
it  seems  that  most  neck  pains  and  parsesthesise  are  placed  in  the  areas 
supplied  by  the  occipitalis  major  and  minor  nerves,  branches  of  the 
second  and  third  cervical  nerves.     (Fig.  75.) 

Cer  vice -occipital  Pains. — There  are  practically  only  a  few  neuralgias 
which  may  be  considered  to  have  a  definite  clinical  course  and  to  be 
entitled  to  the  name  of  special  diseases.  The  chief  of  these  are  tri- 
geminal neuralgia,  neuralgia  of  the  brachial  plexus  and  the  neuralgia 
of  the  sciatic  plexus.  The  other  forms  of  neuralgia  are  nearly  always 
symptomatic  or  reflex  pains  or  are  distinct  manifestations  of  a  neuritis 
or  some  injury  or  irritation  of  the  nerves.  Pains  in  the  neck,  therefore, 
are  very  rarely  to  be  classed  under  the  head  of  "cervical"  neuralgia  or 
''cervico-occipital"  neuralgia.  Nevertheless,  there  is  no  region  of  the 
body  in  which  pain  is  more  frequently  complained  of  than  in  the  back 
of  the  neck  and  head,  unless  we  except  the  trigeminal  pains.  The  ex- 
cessive amount  of  pain  experienced  in  the  neck  is  due  to  several  causes. 
The  muscles  of  the  neck  are  continuously  used,  perhaps  more  than  almost 
any  other  muscles,  except  those  of  the  eyes.  The  supporting  of  the  head 
in  the  erect  posture  and  the  movements  of  it  which  accompany  the  use 
of  vision  make  the  functions  of  the  upper  four  cervical  nerves  an  almost 
continuous  performance. 

Whenever  a  group  of  muscles  is  thus  used  to  such  a  continual  extent 
in  function  two  morbid  phenomena  are  apt  to  occur.  One  is  an  ex- 
haustion of  these  muscles,  with  consequent  pain  from  their  fatigue; 
the  other  is  the  development  in  the  muscular  bodies  or  their  connecting 
tissues   and  nerves   of  rheumatic   and   vascular   disturbances — -so  that 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         181 

pains  in  the  neck  are,  as  a  rule,  either  exhaustion  pains  or  rheumatic 
pains. 

There  is,  however,  another  source  of  pathological  disturbance. 
Whenever  a  serous  membrane  is  irritated,  the  muscular  bodies  which 
surround  it  and  by  their  movements  and  arrangements  support  it, 
experience  reflex  disturbances.  This  we  see  exemplified  by  the  pain 
in  the  side  when  the  pleura  is  involved  and  the  pain  about  the  joints 
when  they  are  inflamed.  So  whenever  the  serous  membranes  sur- 
rounding the  brain  become  congested  or  irritated,  there  results  a  reflex 
disturbance  upon  the  muscular  support  of  the  skull  in  which  the  brain 
is  enclosed. 

Whenever,  then,  by  a  persistent  over-use  of  the  brain,  there  occur 
vascular  changes  of  fatigue,  the  neck  muscles  show  it  in  a  reflex  irri- 
tability and  various  accompanying  sensory  disturbances.  So  in  the 
beginning  of  meningitis  we  find  the  pain  in  the  neck  one  of  the  earliest 
of  the  storm  signals  sent  out. 

Etiology. — ^Pains  in  the  back  of  the  head  and  neck  occur  in  migraine, 
spinal  irritation  and  neurasthenia,  as  a  result  of  eye-strain,  as  a  true 
neuralgia  and  as  a  symptom  of  brain  tumor,  meningitis  and  from  a 
rheumatic  inflammation  of  the  neck  muscles  and  nerve.  Trauma,  spinal 
tumors,  local  disease  of  the  vertebrae  and  herpes  zoster  are  causes  of 
cervical  pains.     Cervical  neuralgia  may  occur  in  tabes. 

Symptoms. — Migrainous  neck  pain  is  described  elsewhere.  It 
is  a  one-sided  trouble  and  periodical  in  type.  In  spinal  irritation  the 
pain  is  central  or,  perhaps,  shifting;  it  is  especially  characterized  by  a 
sharp,  boring  pain  just  below  the  occiput.  With  it  there  may  be  evi- 
dences of  cerebral  congestion  with  vertigo  and  faintnesS;  and  even 
vomiting.  The  boring  pain  is  almost  pathognomonic  of  spinal  irrita- 
tion. In  neurasthenia  which  is  often  associated  with  an  irritable  spine, 
the  pain  is  more  of  a  diffuse,  aching  character. 

In  typical  neuralgia  the  pain  is  usually  unilateral,  paroxysmal  and 
sharp,  sometimes  reaching  the  intensity  of  a  tic  douloureux.  There  are 
tender  points  over  the  exit  of  the  nerves.  The  disease  lasts  for  five  or 
six  weeks.  The  pains  may  alternate  with  or  take  the  place  of  a  trigeminal 
neuralgia.  The  nerves  involved  are  the  great  and  small  occipital  from 
the  second  pair  and  a  branch  from  the  third  pair.  Sometimes  there 
is  a  true  neuritis  due  to  herpes  zoster  and  then  cutaneous  anaesthesia 
is  present. 

Treatment. — Symptomatic  constitutional  treatment  is  indicated,  viz., 
rest,  correction  of  eye-strain,  tonics,  and  when  indicated  the  use  of  anti- 
rheumatics, such  as  the  salicylates.  In  women  pelvic  troubles  should  be 
looked  for.  Locally,  counterirritants,  cupping  and  leeching  are  useful; 
mustard  and  capsicum  pastes  are  often  a  great  relief.     The  ice  bag  also 


182  DISEASES    OF    THE    NEKVOUS    SYSTEM 

is  of  service.  Resection  of  the  occipital  nerves  has  cured  one  obstinate 
case. 

SENSORY  NEUROSES  OF  THE  LOWER  CERVICAL  AND  BRACHIAL  NERVES 

Brachial    Neuralgia     and     Neuritis. — Definition   and   Frequency.^ 

Neuralgia  of  the  brachial  plexus  is  a  disease  characterized  by  severe 
pains  centering  in  the  upper  arm  but  usually  involving  the  whole  up- 
per extremity  and  shoulder;  it  runs  a  course  of  several  months  and  is 
due  to  irritation  with  congestion  of  the  trunks  of  the  brachial  plexus 
and  its  roots  of  origin.  This  irritation  does  not  usually  reach  the  degree 
of  neuritis,  and  the  disease  does  not  show  the  paralysis  and  atrophy, 
anaesthesia  and  the  vasomotor  symptoms  of  neuritis,  as  a  rule.  This 
form  of  neuralgia,  even  excluding  the  cases  of  traumatic  neuritis,  is 
now  by  no  means  a  rare  disease.  Among  the  neuralgias  brought  to  the 
attention  of  the  neurologist  it  ranks  second,  coming  after  the  trifacial 
neuralgias  and  followed  in  frequency  by  the  sciaticas. 

Total  cases  of  arm  pains 79 

Total  brachial  neuralgias 41 

Arm  pains  associated  with  distinct  neuritis 15 

Occupation  neuroses  with  dominant  arm  pains 16 

Hysterical  arm  pains 4 

Palmar,  digital  and  hand  pains  due  to  local  or  reflex  causes ...  6 

Etiology. — ^Brachial  neuralgia  occurs  oftenest  in  persons  in  middle 
life,  ranging  from  thirty-five  to  fifty.  When  it  occurs  in  young  people 
it  is  (like  the  other  neuralgias)  more  often  of  the  hysterical  type,  or 
at  least  associated  with  those  persons  who  are  neurotic  and  over-sen- 
sitive. Besides  having  an  hereditary  neurotic  history  as  the  underlying 
tendency,  there  is  almost  always  a  history  of  severe  emotional  strain — 
loss  of  friends,  sickness  in  the  family  or  worry  over  complications  of 
domestic  Hfe.  Sometimes,  in  addition,  there  is  some  physical  injury 
or  some  acute  sickness.  In  two  cases  I  have  seen  it  follow  profuse 
hemorrhages.  In  some  cases  it  is  due  to  inordinate  use  of  the  arms 
in  simple  manual  work,  like  embroidery  or  knitting;  but  this  seems 
to  me  rather  unusual.  A  mild  form  of  brachial  neuralgia  occurs  in 
women  as  the  result  of  carrying  a  heavy  skirt,  and  it  is  not  unlikely  that 
this  kind  of  work  (skirt  carrying)  and  the  use  of  the  arms  in  dressing  the 
hair  bring  on  neuralgia  in  predisposed  cases. 

Brachial  neuralgias  are  seen  relatively  oftener  in  the  better  classes 
than  in  dispensary  or  hospital  patients.  They  occur  oftener  in  women 
than  in  men  in  the  proportion  of  about  three  to  one.  This  is  contrary 
to  most  statistics,  because,  as  I  believe,  these  statistics  include  many 
frankly  traumatic  and  surgical  cases.     There  is  often  a  predisposing 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         183 

neurotic  or  rheumatic  taint,  and  sometimes  perhaps  an  autotoxsemia. 
Brachial  neuralgia  occurs  in  tabes  dorsalis  and  as  a  symptom  in  other 
organic  diseases.  In  fine,  the  etiology  of  brachial  neuralgia  has  always 
one  or  more  of  three  factors:  neurotic  constitution,  exhaustion  from 
occupation  or  trauma  and  some  endogenous  toxsemic  irritation. 

Pathology. — The  common  form  of  arm  pain  is  usually  designated  as 
a  neuralgia,  though  there  is  probably  some  low  grade  of  inflammatory 
process  in  the  sheaths  of  the  nerves.  If  it  is  desired  to  use  the  term 
''neuritis,"  I  do  not  know  that  serious  objection  could  be  made.  So  far 
as  I  am  aware,  no  post-mortem  examinations  have  been  made  of  the 
nerves  of  persons  suffering  from  this  condition,  except  of  certain  acute 
hemorrhagic  cases.  If  we  may  infer  concerning  it  by  analogy,  from  con- 
ditions seen  in  sciatica,  the  existence  of  perineuritic  irritation  and  perhaps 
shght  exudate,  is  probable.  Probably  sometimes  the  inflammation  is 
not  so  much  in  the  nerve-sheaths  as  in  the  muscular  and  connective  tissues 
about  it,  and  that  there  is  a  myositis  as  well  as  secondary  neuritis.  In 
using  the  word  "brachial  neuralgia"  I  include  both  the  neuralgias,  with 
no  objective  symptoms,  and  the  distinctly  neuritic  cases,  of  non-surgical 
origin. 

Symptoms. — The  onset  is  rather  sudden,  but  there  may  be  severe 
preliminary  aching  in  the  arm  for  a  few  days,  and  sometimes  there 
are  short  preliminary  or  abortive  attacks.  Usually,  however,  the 
patient  wakes  at  night  or  notices  in  the  morning  a  distinct  and  severe 
pain  involving  the  upper  arm  and  shoulder  or  perhaps  the  whole  arm. 
The  pain  usually  is  most  acute,  however,  on  the  inner  and  front  side 
of  the  arm  and  in  the  back  between  the  shoulders.  It  is  very  intense 
and  runs  down  the  forearm  and  into  the  fingers,  involving  sometimes 
the  whole  hand,  but  usually  only  the  first,  second  and  third  fingers. 
It  is  not  a  darting,  shooting  pain,  but  seems  to  be  one  that  is  general 
and  diffuse,  involving  for  a  time  the  whole  arm  with  a  pain  of  paralyzing 
intensity.  The  pains  exacerbate,  coming  on  usually  at  night  more 
severely,  or  more  in  the  morning,  and  always  more  after  exertion. 
Movement  makes  the  suffering  worse;  but  the  arm  can  be  handled 
gently  without  much  pain.  Some  suffering  is  present  nearly  all  the  time, 
often  robbing  the  patient  of  sleep ;  but  it  may  let  up  for  a  few  hours  during 
the  day  and  then  comes  back  again  with  paroxysms  of  great  intensity 
lasting  for  one  or  two  hours. 

Many  patients  try  at  first  to  work  off  the  pain  by  exercise,  thinking 
it  a  form  of  rheumatism,  or  they  get  a  masseur  who  rubs  the  arm,  and, 
as  a  rule,  makes  it  worse.  There  are,  however,  at  times,  attacks  that 
are  short  and  abortive.  I  have  known  some  to  last  three  or  four  days. 
and  in  these  instances  the  massage  or  the  doctor  get  the  credit  for  a  thera- 
peutic triumph  entirely  undeserved.     Usually  the  pains  progress  and 


184 


DISEASES    OF    THE    NERVOUS    SYSTEM 


continue  for  two  or  three  weeks  until  the  trouble  is  pretty  firmly  estab- 
lished, continuing  then  for  two  or  three  months. 

When  the  pain  first  comes  on  there  are  no  objective  changes  in  the 
arm.  It  looks  normal  and  is  simply  tender  and  sore  to  the  touch.  Later 
the  arm  becomes  a  little  swollen  and  the  fingers  somewhat  edematous, 
and  there  is  slight  flabbiness  of  the  tissues,  showing  vasomotor  change. 

In  the  typical  neuralgias  there  is  rarely  much  more  than  this.  If  it 
is  a  genuine  neuritis,  atrophies  and  paralyses  gradually  develop.  In 
brachial  neuralgias  proper  the  changes  in  the  arm  are  only  slight — the 
grip  of  the  hand  becomes  weak,  the  elbow-jerk  is  a  little  exaggerated  at 
first,  muscular  irritability  is  increased  and  then  diminished, "  and  there 
is  no  anaesthesia. 


Fig.  78. — The  pains  and  painful  points  of  brachialgia. 

Examination  shows  points  of  tenderness  along  the  course  of  the 
nerve  on  the  inner  side  of  the  arm  at  the  elbow  and  over  the  deltoid. 
There  is  also  a  point  of  tenderness  between  the  scapulae  about  at  the 
level  of  the  second  or  third  dorsal  vertebra.  This  is  very  painful  and  is 
characteristic.  Stretching  out  the  arm  and  drawing  upon  the  brachial 
plexus  brings  out  pain,  just  as  it  does  in  the  extension  of  the  leg  in  sciatica. 
Later  there  is  also  weakness  of  response  to  the  elbow-jerk,  just  as  in  the 
tendo  achillis  in  the  later  stages  of  sciatica.  The  tender  points  that  one 
finds  in  brachial  neuralgia  are  by  no  means  always  identical  with  the 
tender  points  of  Valleix.  They  vary  somewhat  and  only  correspond  in  a 
general  way  to  the  distribution  of  the  cutaneous  nerves  (Fig.  78). 

It  will  be  found,  as  we  note  the  neuralgias  from  the  back  of  the  neck 
down  to  the  hand,  that  pains  in  these  different  segments  are  associated 
with  painful  points  along  the  course  of  the  spine.  For  example:  In 
occipital  neuralgia  there  will  be  a  well-marked  tender  point  close  up  to 


SENSORY    NEUROSES    OF   THE    CEREBROSPINAL    NERVES         185 

the  base  of  the  skull  over  the  second  or  third  cervical  spines.  With  a 
cervicobrachial  neuralgia  the  point  moves  down  to  near  the  first  or 
second  dorsal.  With  a  brachial  neuralgia  the  spinal  tender  point 
moves  to  the  neighborhood  of  the  third  or  fourth  dorsal.  These  spinal 
tender  points  are  quite  characteristic  of  neuralgias  of  the  upper  cervical 
plexus,  and  the  collaterals  of  the  brachial  plexus. 

Diagnosis. — In  the  chronic  and  less  severe  types  of  arm  pain  one  may 
be  easily  misled  in  diagnosis.  The  first  and  obvious  name  given  to  an 
arm  pain  is  "rheumatism."     The  patient  is  always  treated  first  for  this. 

It  is  safe  to  say  that  arm  pains  are  never  purely  rheumatic,  unless 
there  is  found  some  objective  evidence  of  myositis,  arthritis,  or  periar- 
thritis. The  most  difficult  thing  is  to  distinguish  between  real  neuritis 
of  high  grade  and  neuralgia.  Neuritis  has  become  a  popular  diagnosis 
nowadays,  and  patients  talk  very  glibly  about  the  term.  But  a  neuritis 
cannot  be  recognized  except  by  some  objective  signs.  There  must  be 
pain  and  also  tenderness  along  the  nerve;  there  must  be  definite  areas  of 
hyperaesthesia  or  anaesthesia,  muscular  weakness,  and  perhaps  atrophy 
and  electrical  changes.  There  must  be  some  of  these  symptoms  in  an 
inflammatory  process  that  last  three  to  six  months. 

In  about  half  of  the  cases  no  such  objective  symptoms  are  present. 
The  condition  is  not  one  of  actual  inflammation,  but  of  exhaustion, 
and  in  the  majority  of  cases  brachial  neuralgia  is  an  exhaustion  neurosis 
with  some  rheumatic  or  metabolic  irritation  of  the  nerves  in  addition. 

When  we  flnd  a  herpes  along  with  arm  pain  we  know  that  we  have  an 
inflammation  of  the  spinal  ganglion  and  secondary  neuritis  and  that  the 
process  is  due  to  an  infection. 

Treatment.- — The  treatment  of  brachial  neuralgia  is  fundamentally 
that  of  rest.  This  must  be  secured  by  a  sling,  and,  if  necessary,  by 
spHnts.  In  a  good  proportion  of  cases  some  relief  is  gotten  by  the 
salicylates,  especially  aspirin,  but  they  must  be  given  in  very  large  doses, 
just  as  for  acute  rheumatism. 

No  massage  nor  other  mechanical  treatment  should  be  given  at  first. 
But  hot  air,  baking,  hot  pads,,  hot  applications  of  mud  or  flannel  should 
be  used.  The  patient  must  understand  that,  as  a  rule,  it  often  takes 
ten  or  twelve  treatments  to  accomplish  results. 

After  a  course  of  salicylates,  tonics  can  be  given.  I  do  not  know 
any  drug  that  is  of  any  special  value  unless  it  is  strychnine,  in  massive 
doses,  but  of  its  utility  I  am  sure  in  chronic  cases. 

Arm  pains,  which  once  were  due  to  neuritic  conditions,  sometimes 
become  habit  pains;  the  patient  has  a  ''constitutional  armache,"  just 
as  some  have  constitutional  headache.  The  best  and  only  treatment 
for  these  patients  is  to  ignore  the  trouble  absolutely.  When  the  pains 
have  become  chronic,  i.e.,  after  four  to  six  weeks,  massage  and  electricity 


186 


DISEASES    OF    THE    NERVOUS    SYSTEM 


do  some  good.  The  patient  gets  well  anyway  in  three  to  six  months  as 
a  rule. 

The  disease  may  recur,  but  this  is  rather  rare,  and  only  in  about 
10  per  cent,  of  my  cases. 

It  is  rarely  double,  and  when  so  is  invariably  an  exhaustion  or  psy- 
chogenous  neuralgia,  if  we  can  exclude  organic  disease. 

Pains  in  the  Forearm  and  Fingers. — There  are  rarely  true  neuralgic 
or  neuritic  pains  confined  to  the  forearm  alone.  Here  we  have  only 
the  ulnar  pains  following  the  course  of  the  ulnar  nerve,  and  very  char- 
acteristic radial  pains  following  the  back  of  the  arm  to  the  fingers,  and 
least  frequently  median  nerve  pains.  Sometimes  the  whole  hand  is 
involved  in  neuralgic  pain,  but  this  is  usually  hysterical.     The  hand  and 


Fig.  79. — The  location  of  reflex  heart  pains. 

fingers  have  paraesthesias  and  local  pains  due  to  central  or  local  disease, 
but  no  neuralgia  except  in  tabes  dorsalis. 

Heart  Arm-pains. — Cardiac  arm  pains  are  not  very  prominent 
factors  in  the  ordinary  heart  disease  of  the  hospitals,  and  do  not  appear 
so  dominant  among  the  laboring  classes.  Almost  always  in  persons  who 
have  a  cardiac  disease  and  who  have  pains  in  the  arm  there  is  a  decidedly 
neurotic  element.  This  means,  that  the  nervous  system  being  more 
sensitive  and  unstable,  the  irritating  impulses  from  the  myocardium 
radiate  more  freely  and  arouse  disturbances  in  consciousness  more 
easily.  These  cardiac  arm  pains,  are  generally  associated  with  some 
precordial  pain,  not  infrequently  with  some  pain  near  the  scapula,  and 
also  pains  on  the  inner  side  and  middle  of  the  upper  arm  and  middle  of 
the  forearm.  They  rarely  extend  into  the  fingers.  Sometimes  there  is 
distinctly  a  pain  in  the  right  arm  instead  of  the  left.  The  accompanying 
diagram  shows  the  usual  localization  of  these  pains  (Fig.  79).     There 


SENSOKY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES 


187 


is  generally  a  feeling  that  the  pain  comes  from  the  left  side  and  runs  from 
there  into  the  arm.  The  cause  of  this  reflex  disturbance  is  generally 
attributed  to  the  fact  that  the  third  or  lower  cardiac  ganglion  of  the 
cervical  sympathetic  sends  fibres  which  communicate  with  the  first 
dorsal  nerve,  which  nerve  supplies  the  inner  side  of  the  arm  (Fig.  80). 


a^;;:^;^^w-  *  •■' 


Fig.  80. — Showing  the  relation  of  the  third  cervical  and  first  thoracic   ganglion 
(blended  together)  with  the  brachial  plexus. 

THE  SENSORY  NEUROSES  OF  THE  INTERCOSTAL  NERVES 

These  are  chiefly  intercostal  neuralgia,  symptomatic  side  pains, 
and  herpes  zoster.  Paralyses  and  anaesthesias  occur  in  connection  with 
vertebral  and  spinal-cord  diseases. 

Intercostal  Neuralgia. — Intercostal  neuralgias  are  quite  rare.  They 
occur  in  chronic  lead-poisoning,  in  the  neuralgic  form  of  tabes,  follow- 
ing herpes  zoster,  and  in  hysteria.  Neuralgic  pains  in  the  side  due 
to  some  organic  disease  irritating  the  intercostal  nerves  are,  however, 
common.  They  occur  in  vertebral  and  spinal  cord  disease  (tumors 
and  syphilis)  in  local  disease  irritating  the  nerve,  fracture  of  the  ribs, 
pleurisy,    tumors,    aneurism,    myositic    and   arthritic    processes,  angina 


188  DISEASES    OF    THE    NERVOUS    SYSTEM 

pectoris,  and  trauma  of  the  nerves.     Reflex  pains  from  disease  of  the 
viscera  are  common  (see  Fig.  68). 

Symptoms. — -The  pain  in  typical  cases  is  sharp  and  stabbing,  but  not 
much  increased  by  respiratory  movements.  There  are  tender  points 
at  the  seat  of  pain,  which  is  usually  greatest  over  the  side  at  the  exit  of 
the  lateral  nerve  branches.  Often  a  tender  point  is  felt  over  the  exit  of 
the  dorsal  or  of  the  anterior  branch.  It  is  rare  to  find  all  three 
points. 

The  sixth  to  tenth  nerves  are  those  oftenest  involved.  The  left  side 
is  more  susceptible  than  the  right. 

Probably  one-half  the  pains  in  the  side  are  myalgic  in  nature,  and 
should  be  classed  as  such.  These  pains  can  be  distinguished  by  the 
history  of  their  origin  and  of  rheumatic  influences,  by  their  diffuseness 
and  dullness,  by  the  great  tenderness  on  pressure,  and  the  pain  pro- 
duced on  taking  a  deep  breath.  There  is  another  considerable  propor- 
tion of  cases  in  which  the  pains  are  mainly  neuritic,  but  yet  there  are 
some  eivdences  of  muscular  complications.  Some  of  these  pains  are 
reflex. 

In  the  third  class  of  cases  there  is  the  pure  stabbing  neuralgia.  The 
diagnosis  is  based  on  the  exclusion  of  pleurisy,  visceral  disease,  tabes, 
rheumatic  causes,  by  the  character  of  the  pain  and  the  presence  of 
tender  points. 

Treatment.  ^In  all  cases  the  heart,  pleura,  stomach,  and  pelvic 
organs  must  be  examined,  and  any  disorder  relieved.  If  there  is  a  rheu- 
matic and  muscular  element,  salicylates  or  the  analgesics  should  be  given. 
Apply  heat  and  secure  rest  by  adhesive  straps. 

Mammary  neuralgia  {mastodynia)  is  a  form  of  intercostal  neuralgia 
involving  the  anterior  and  lateral  branches  of  the  three  or  four  upper 
dorsal  nerves. 

Etiology. — It  may  be  caused  by  local  disorders,  or  it  may  be  a  func- 
tional or  a  traumatic  neuralgia.  The  causes  in  the  latter  class  are 
pendent  breasts,  pressure  from  badly-fitting  corsets  and  injury.  Mam- 
mary neuralgia  also  occurs  in  hysterical  women  and  young  girls  sexually 
precocious;  it  may  occur  in  pregnancy  and  during  lactation.  Many 
mammary  pains  are  due  simply  to  local  disorder  of  the  gland. 

Symptoms. — Mammary  neuralgia  is  unilateral,  often  very  severe, 
and  if  it  occurs  in  middle  life  is  liable  to  cause  much  mental  depression 
from  fear  of  cancer. 

The  treatment  depends  upon  the  cause.  It  requires  general  tonic 
measures  and  attention  to  reflex  agencies  and  to  the  proper  support  and 
protection  of  the  gland. 

Herpes  Zoster  (Shingles). — This  is  an  acute  dermatitis,  secondary 
to  a  ganglionitis.     It  may  attack  any  of  the  cerebrospinal  ganglia. 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL   NERVES         189 

Etiology. — Its  predisposing  causes  are  wounds,  drug  habits,  rheu- 
matic, gouty  and  syphiHtic  poisons  and  emotional  inlEluences.  The 
active  cause  is  in  most  cases  an  infection,  and  the  disease  sometimes 
is  almost  epidemic.  The  trouble  is  not  infrequent  in  tabes  dorsalis. 
The  inflammation  affects  not  only  the  nerves,  but  the  spinal  ganglia, 
and  especially  the  latter,  so  that  the  condition  has  been  called  a  pos- 
terior poliomyelitis  (Head).  Examination  of  the  cerebrospinal  fluid 
often  show  a  lymphocytosis. 

Symptoms. — -It  begins  gradually  with  the  development  of  pain 
and  a  herpetic  eruption  upon  one  side  of  the  trunk.  It  generally  in- 
volves the  lower  dorsal  nerves.  The  eruption  follows  the  course  of 
the  nerve,  rarely  extending  to  the  opposite  side.  The  pain  gradually 
subsides,  and  the  disease  itself  runs  its  course  in  one  or  two  weeks.  Some- 
times it  leaves  the  patient  with  a  chronic  neuralgia  lasting  for  months. 

Treatment. — -Local  anodynes  and  protective  ointments  should  be  ap- 
plied (1  per  cent,  mixture  of  cocaine  in  lanolin).  Antirheumatics 
and  analgesics  are  to  be  administered  internally.  The  free  use  of  the 
analgesic  coal-tar  products  appears  to  lessen  the  severity  and  length  of 
the  disease.     In  chronic  cases  very  large  doses  of  strychnine  are  indicated. 

SENSORY  NEUROSES  OF  THE  LUMBAR  NERVES 

Painful  conditions  center  about  the  lumbar  region  and  hips  more  than 
in  any  other  region  except  the  head.  Most  of  these  pains  are  myalgic, 
and  arthritic,  or  are  reflex  from  pathological  conditions  in  the  pelvis  and 
lower  abdominal  cavity.     Such  pains  are  diffuse  and  generally  bilateral. 

These  various  pains  are  grouped  clinically  under  the  head  of: 

1.  Lumbago. 

2.  Spinal  irritation  (neuro -myalgia). 

3.  Arthritis  of  various  types  and  joints,  from  gonococcic  and  other 
infections. 

4.  Reflex  pains. 

This  leaves  few  disorders  of  the  lumbar  nerves  that  are  strictly  neural 
in  origin.  They  are  lumbo-abdominal  neuralgia,  meralgia  and  anterior 
crural  neuralgia. 

Lumbo-abdominal  Neuralgia. — ^The  upper  two  lumbar  nerves  are 
almost  entirely  sensory.  When  they  are  the  seat  of  a  neuralgia,  there  is 
sharp  pain  in  the  groin,  back  and  buttocks,  extending  over  the  hypo- 
gastrium  or  genitals  on  one  side.  The  pain  in  the  back,  however,  is  often 
bilateral.  Painful  points  may  be  found  after  a  time,  as  in  intercostal 
neuralgia.  Sometimes  the  pain  is  located  in  the  side  of  the  penis  (penile 
neuralgia; . 

Crural  neuralgia  of  the  long  lumbar  branches  is  called  femoral  or 


190 


DISEASES    OF    THE    NERVOUS    SYSTEM 


crural.  When  these  nerves  are  subject  to  a  lesser  irritation,  causing  sensa- 
tions of  numbness  and  pricking  along  the  thigh,  the  condition  is  called 
meralgia.  In  true  neuralgia,  the  patient  complains  of  pain  in  the  front 
of  the  knee  and  the  anterior  and  outer  parts  of  the  thigh,  but  has  no  pain 
posteriorly  and  none  below  the  knee.  The  internal  branches  of  the 
anterior  crural  nerve  do  not  seem  to  be  affected,  while  the  middle  and 
external  cutaneous  branches  and  the  genito-crural  nerve  are  involved. 

Reflex  Pains. — Disease  of  the  hip  or  of  the  sacro-iliac  joint  or  vertebrae 
may  cause  a  reflex  pain  in  the  obturator  nerve,  localized  especially  in  the 


Fig.  81. — Areas    of   cutaneous    hypersesthesia   in   disease   of   the   stomach.     Sixth, 
seventh,  eighth  and  ninth  dorsal  nerve-segments.     {Head — Fraenkel.) 


knee  and  back  of  this  joint.  The 
branches,  causing  a  symptomatic 
its  adnexse  are  especially  liable  to 
Lesions  of  the  appendix,  kidney, 
nerves.  Diseases  of  the  external 
pains  upon  the  sacral  nerves.  I 
inguinal  and  hypogastric  nerves 


fcetal  head  sometimes  compresses  these 
neuralgia.  Disorders  of  the  womb  and 
cause  reflex  pain  in  the  lumbar  nerves, 
ureters  also  reflect  pains  to  the  lumbar 
genitals  and  bladder  more  often  reflect 
n  renal  colic  pains  are  felt  in  the  iho- 
Local  disease  of  the  psoas  muscle  or 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         191 

iliacus,  in  the  neighborhood  of  Poupart's  hgament,  causes  pains  in  the 
lumbar  nerves.     (See  Head  Zones,  Figs.  81,  82,  83,  84,  85). 

Pains  over  the  sacro-ihac  synchondrosis  occur  in  rheumatic  inflam- 
mation of  these  joints.  Goldthwaite  has  shown  that  in  certain  injuries 
there  may  be  a  shght  dislocation  and  sprain  of  these  joints.  In  these 
cases  if  the  patient  lie  on  his  back  and  the  leg  lifted  in  the  extended 
position,  great  local  pain  is  elicited  and  the  patient  cannot  voluntarily 
raise  the  extended  leg. 

Diagnosis. — Lumbar  neuralgia  is  distinguished  from  lumbago  by 
the  unilateral  position,  the  distribution  and  paroxysmal  character  of 
the  pain  and  lack  of  severe  suffering  on  motion  and  pressure;  the  tender 
points  and  the  absence  of  any  organic  disease.  Lumbago  comes  on 
suddenly,  with  a  history  of  exposure  or  strain,  is  bilateral  and  confined 
to  a  single  group  of  muscles,  which  are  tender  on  deep  pressure.  In 
lumbar  strain  the  onset  is  also  sudden,  with  a  history  of  injury,  great 
local  tenderness  and  evidences  of  trauma.  Most  chronic  lumbar  pains 
are  reflex  or  symptomatic  and  the  main  object  of  diagnosis  is  to  find  the 
cause. 

The  treatment  is  the  removal  of  the  cause.  The  frequent  presence 
of  pelvic  disease,  of  sacro-iliac  joint  disease,  and  of  strain  and  a  rheu- 
matic history  must  be  borne  in  mind. 

Head's  Zones. — In  cases  of  acute  or  subacute  inflammation  of  the 
viscera,  areas  of  skin  hypersesthesia  usually  appear  in  certain  definite 
segments  corresponding  to  the  organs  diseased.  The  accompanying 
figures  are  furnished  me  by  Dr.  Jos.  Fraenkel  from  cases  observed  by 
him.  The  testing  for  these  hypersesthetic  areas  has  sometimes  diagnostic 
value. 

Sciatica  (Neuralgia  of  the  Sciatic  Nerve,  Sciatic  Neuritis). — This  is 
a  form  of  neuralgia  occurring  in  middle  life  and  characterized  by  intense 
pain  in  the  course  of  the  sciatic  nerve.  A  large  proportion  of  the  cases 
is  due  to  neuritis. 

Etiology. — The  disease  occurs  three  times  as  often  in  men  as  in  women, 
and  is  the  only  neuralgia  of  which  this  can  be  said.  Most  cases  in  this 
country  occur  between  the  ages  of  forty  and  fifty;  next  between  thirty  and 
forty. 

The  gouty  and  arthritic  diathesis,  and  occupations  which  lead  to 
exposure  and  strain,  predispose  to  the  disease.  It  is  not  rare,  therefore, 
among  laboring  men.  In  younger  persons  a  neurotic  constitution  pre- 
disposes to  the  disease,  and  in  this  class  the  trouble  is  more  truly  of  a 
reflex  and  neuralgic  character  and  less  of  a  neuritis. 

Most  cases  occur  in  the  autumn  and  winter.  The  exciting  causes 
are  constipation,  pressure  from  hard  seats,  exposure,  muscular  strain 
from  heavy  work  and  pelvic  disorders.     Symptomatic  sciatica  may  be 


192 


DISEASES    OF    THE    NERVOUS    SYSTEM 


caused  by  the  pressure  of  pelvic  tumors,  injury  to  the  nerves,  vertebral 
and  spinal  disease;  sciatica  occurs  in  paralysis  agitans  and  in  diabetes 
and  in  phthisis.  In  elderly  persons  of  a  rheumatic  constitution  inflam- 
matory processes  about  the  hip-joint  complicate  or  cause  the  neuralgia. 
Symptoms. — The  disease  begins  rather  suddenly.  Pain  is  felt  in  the 
back  of  the  thigh,  running  down  the  leg  in  the  course  of  the  nerve. 
Generally  it  is  most  marked  in  the  thigh,  extending  up  often  into  the 
lumbar  region.     Sometimes  the  disease  begin  like  a  lumbago;  more  rarely 


Fig.  82.  Fig.  83. 

Fig.  82. — Area  of  cutaneous  hypersesthesia  in  a  case  of  cholelithiasis  and  chole- 
cystitis.     (J.  Fraenkel.) 

Fig.  83. — Area  of  cutaneous  hypersesthesia  in  a  case  of  cholecystitis.    {J.  Fraenkel.) 


pain  is  first  felt  in  the  calf  or  foot.  The  pain  is  increased  by  motion,  and 
the  patient  holds  himself  in  a  constrained  position.  The  pelvis  is  tilted 
up  toward  the  sound  side  and  the  trunk  inclined  over  to  the  diseased  side. 
After  a  time  this  leads  in  some  cases  to  a  characteristic  deformity  (sciatic 
scoliosis)  in  which  the  convexity  of  the  curve  of  the  vertebral  spines  is 
directed  toward  the  diseased  side.  The  pain  is  almost  continuous,  with 
paroxysms  of  great  severity,  which  often  occur  at  night.     During  these 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES 


193 


paroxysms  the  pain  is  sharp,  burning  and  lancinating.  In  the  interval 
it  is  dull.  Besides  the  pains  the  patient  suffers  from  feelings  of  numbness, 
tingling,  and  a  sense  of  coldness  and  weight  in  the  affected  limb.  There 
are  almost  always  tender  points  over  the  course  of  the  nerve.  These 
may  be  found  at  the  sciatic  notch,  at  the  middle  of  the  hip,  behind  the 
knee,  just  below  the  head  of  the  fibula  in  the  middle  of  the  calf,  behind  the 
external  malleolus  and  on  the  back  of  the  foot  (Fig.  86). 


Fig.  84.  Fig.  85. 

Fig.  84. — Area  of  cutaneous  hypersesthesia  in  appendicitis.     (/.  Fraenkel.) 
Fig.  85. — Area  of  cutaneous  hypersesthesia  in  a  case  of  salpingitis.      (/.  Fraenkel.) 

A  pain  running  up  the  back  of  the  thigh  may  be  caused  by  pressure 
over  the  back  of  the  knee  when  the  leg  is  extended  at  a  little  more  than  a 
right  angle.  This  is  diagnostic  (Gowers).  If  the  patient  lies  on  his 
back  and  the  leg  is  kept  extended,  and  then  the  whole  limb  brought  slowly 
up  until  it  is  at  an  acute  angle  with  the  trunk,  a  sharp  pain  in  the  sciatic 
notch  is  felt;  this  too  is  diagnostic.  Anaesthesia  over  the  course  of  the 
nerves  occurs  very  rarely.  When  present,  it  indicates  a  severe  neuritis 
or  injury  to  the  nerve.  Muscular  wasting  and  weakness  occur  after  a 
time,  and  in  old  and  severe  cases  partial  electrical  degeneration  reactions 

13 


194 


DISEASES    OF    THE    NERVOUS    SYSTEM 


may  be  observed.  The  ankle-jerk  is  usually  abolished,  but  the  other 
reflexes  remain  normal  or  nearly  so.  Herpetic  eruptions  over  the  course 
of  the  nerve  occur  in  rare  cases.  The  affected  limb  usually  feels  colder 
and  shows  evidence  of  enfeebled  vasomotor  supply. 

The  disease  usually  lasts  two  or  three  months;  not  rarely  it  lasts  six 

months  or  even  a  year  or  more.     It  has 

been  known  to  extend  slowly  upward 
and  involve  the  sacral  plexus  or  even  the 
spinal  cord. 

Pathology. — Only  twelve  autopsies  are 
on  record.  There  has  been  found  in  some 
cases  a  thickening  of  the  nerve  and  a 
gelatinous  exudate  in  the  perineural 
sheath,  the  fluid  not,  however,  contain- 
ing evidence  of  cellular  proliferation  (J. 
R.  Hunt).  The  arteries  are  thickened 
and  sclerosed.  The  evidence  points  to  the 
presence  in  ordinary  sciatica  of  a  perineu- 
ritis with  exudate  often  of  gouty  or  rheu- 
matic origin. 

Diagnosis. — Sciatica  has  to  be  distin- 
guished from  hip-joint  disease,  dislocation 
and  sprains  of  the  sacro-iliac  synchondro- 
sis, organic  disease  of  the  cauda  equina  or 
cord,  muscular  pains  in  the  hip  and  leg 
(rheumatic  myositis)  and  from  pains 
caused  by  tumors.  A  true  sciatic  neural- 
gia ought  also  to  be  distinguished  from 
sciatic  neuritis.  A  consideration  of  the 
facts  already  given  ought  to  make  the 
diagnosis  not  difficult.  Pure  sciatic  neu- 
ralgia occurs  in  early  life  and  is  not  ac- 
companied by  much  local  tenderness. 
There  is  no  paralysis  or  wasting  of  the 
limb  or  anaesthesia.  Double  sciatica  is 
most  always  symptomatic  of  diabetes  or 
organic  disease. 

Prognosis. — Almost  all  cases  get  well 
in  from  three  to  six  months.  Severe  attacks  in  people  over  forty  are 
the  most  intractable.     Relapses  occur,  but  not  as  a  rule. 

Treatment. — In  bad  cases  which  are  seen  early,  the  most  important 
indication  is  rest.  The  patient  should  be  put  to  bed,  and  the  whole  lower 
extremity  secured  in  a  splint.     Ice  bags  or  heat  should  then  be  applied 


Fig.    86. — Painful   joints  in 
sciatica. 


SENSOEY    NEUROSES    OF   THE    CEREBROSPINAL   NERVES        195 

over  the  course  of  the  nerve.  A  blue  pill  (gr.  v.)  may  be  given  twice 
daily  at  first.  In  less  severe  or  older  cases  the  baking  process  may  be 
used,  or  large  blisters  applied  over  the  nerve  in  the  thigh,  and  the 
application  repeated  in  a  week.  If  there  is  a  rheumatic  history,  potas- 
sium salicylate  or  iodide  should  be  given  in  full  doses.  The  bowels 
must  be  freely  opened.  Hypodermatic  injections  of  morphine  or  cocaine 
(gr-  3"i)  may  be  needed  for  a  few  days,  the  cocaine  being  repeated  if 
necessary.  When  the  disease  has  become  more  chronic,  a  strong  gal- 
vanic current  may  be  given  daily  with  large  electrodes,  one  over  the 
lumbar  region  or  sciatic  notch,  the  other,  which  should  be  the  positive 
pole,  over  the  leg  and  foot.  As  so-called  specific  remedies  we  have 
oil  of  turpentine  in  closes  of  fifteen  drops  t.  i.  d.,  and  this  may  be  advan- 
tageously combined  with  oil  of  gaultheria.  Massive  doses  of  antifebrin 
or  antipyrin  sometimes  stop  the  pains  (gr.  x.,  q.  2  h.).  There  are  a 
great  many  local  remedies  which  at  times  prove  useful.  Among  these 
are  mustard  plasters,  menthol,  chloroform  liniment,  and  the  actual 
cautery.  Bandaging  the  limb  in  sulphur  to  which  a  little  menthol  is 
added  is  often  very  efficacious.  Kneading  the  nerve  with  a  glass  rod 
and  an  anodyne  ointment  is  sometimes  beneficial.  Massage  is  useful 
after  the  acute  stage  is  passed.  Very  little  can  be  expected  from  nerve- 
stretching,  but  it  may  be  tried  as  a  last  resort.  If  tried,  however,  great 
caution  should  be  exercised  in  pulling  on  the  nerve.  Not  over  thirty 
to  forty  pounds  pull  should  be  used.  The  operation  of  cutting  down 
on  the  nerve  and  dissecting  off  the  sheath  for  a  space  of  several  inches 
has  been  tried.  The  injection  of  a  normal  saline  solution  about  the 
nerve  has  been  recommended. 

Plantar  Neuralgia. — In  rare  cases  the  pain  of  sciatic  neuralgia  is 
limited  to  the  plantar  nerves,  and  is  accompanied  by  parsesthesia  and 
even  anaesthesia  of  this  region.  The  condition  here  is  probably  a  neuritis 
combined  sometimes  with  arthritic  changes.  Erythromelalgia  may  be 
regarded  as  a  form  of  plantar  neuralgia. 

Erythromelalgia  {red  neuralgia  of  the  feet,  congestive  neuralgia)  is  a 
disease  affecting  both  feet,  and  characterized  by  burning  pains  and 
congestion  of  the  parts. 

The  disease  occurs  usually  in  men  in  middle  life,  after  some  infection 
or  severe  physical  exertion  afoot.  It  is  due  sometimes  to  gouty  habits, 
and  I  have  seen  it  in  patients  who  were  diabetics. 

The  disease  begins  in  the  ball  of  the  foot  or  the  heel  with  burning 
pains.  The  trouble  increases  until  nearly  the  whole  sole  in  the  dis- 
tribution of  the  plantar  nerve  is  involved,  and  the  pain,  though  worse  at 
night,  is  almost  continuous.  It  is  much  increased  by  exertion,  the  feet 
become  very  tender  so  that  standing  or  walking  is  most  painful.  Mean- 
while there  has  developed  with  the  pain  a  flushing  of  the  part  upon 


196  DISEASES   OF   THE    NEEVOUS   SYSTEM 

exertion.  In  bad  cases  the  parts  most  affected  are  continuously  marked 
by  a  dull,  dusky,  mottled  redness,  with  some  swelling.  The  hands 
may  be  slightly  affected.  Slight  injuries  may  cause  blisters  and  even 
ulcerations.  The  congestion  usually  disappears  in  the  horizontal  position 
and  this  also  relieves  the  pain.  The  symptoms  are  worse  in  warm 
weather.  The  disease  is  very  chronic  and,  though  not  dangerous  to  life, 
makes  life  very  miserable. 

Pathology. — In  the  cases  of  erythromelalgia  as  described  by  Mitchell 
and  others,  there  are:  (1)  A  vasomotor  disturbance;  (2)  a  neuritis; 
and  (3)  in  rare  instances,  spinal-cord  disease;  (4)  probably  in  most 
cases  there  is  an  obliterative  arteritis  or  other  form  of  vascular  disease. 

The  diagnosis  must  be  made  from  alcoholic  and  gouty  parsethesia, 
podalgia,  local  disease  of  bone  and  ligaments,  and  from  reflex  pains. 

Treatment. — ^Elevation  of  the  feet  and  applications  of  cold  give 
temporary  relief.  Faradization  has  sometimes  given  help;  oftener  it 
has  not.  There  is  nothing  known  which  gives  permanent  relief.  The 
physician  must  rely  upon  rest,  bandaging,  cold,  anodyne  applications, 
hydrotherapy  and  tonics.  Baking  the  part  is  sometimes  useful  especially 
when  there  is  arteriosclerosis.  The  salicylates,  iodides,  mercury, 
nitrites,  and  mineral  acids  with  strychnine  may  be  given. 

Morton's  neuralgia,  so-called,  is  a  neuralgia  affecting  the  metatarso- 
phalangeal joint  of  the  third  and  fourth  toes,  and  is  due,  it  is  thought, 
to  a  slight  luxation,  with  consequent  pressure  on  a  digital  branch  of 
the  external  plantar  nerve.  It  sometimes  affects  other  toes,  however. 
It  is  not  always  due  to  a  luxation.  Incipient  flatfoot  may  cause  it,  and 
I  have  seen  a  typical  case  in  a  pregnant  woman,  disappearing  after 
confinement.  The  trouble  occurs  generally  in  women,  and  if  there  is  a 
luxation  the  cause  is  external  injury  or  shoe  pressure.  The  treatment  is 
not  very  satisfactory.  It  should  be  directed  to  giving  rest  to  the  foot, 
and  the  avoidance  of  lateral  pressure  on  the  joints  by  wearing  a  broad- 
soled  shoe  with  support  to  the  arch  of  the  foot.  Support  may  also  be 
given  by  a  broad  flannel  bandage.  Amputation  of  the  toe  is  a  very 
certain  remedy. 

Tarsalgia  {'policeman' s  disease)  is  a  painful  affection,  due  probably 
in  most  cases  to  an  incipient  flattening  of  the  foot  and  stretching  of 
the  plantar  ligaments.  Some  have  ascribed  it  to  a  deep-seated  con- 
tusion of  the  adipose  cushion  covering  the  os  calcis.  A  chronic  in- 
flammation of  the  sheath  of  the  tendo  achillis  causes  symptoms  re- 
sembling podalgia.  Probably  the  condition  varies  somewhat  in  different 
cases.  It  is  observed  in  persons  who  have  been  in  the  habit  of  going 
barefoot,  and  have  then  gone  into  the  army  or  taken  civil  positions  oblig- 
ing them  to  stand  or  walk  a  great  deal. 

It  was  noticed  originally  in  the  policemen  of  Paris,  and  cases  have 


SENSORY    NEUROSES    OF    THE    CEREBROSPINAL   NERVES         197 

been  seen  in  this  country.     The  name  tarsalgia  was  given  by  Duchenne. 

Pododynia  may  be  caused  by  a  slight  shortening  or  contraction  of  the 
tendo  achillis  and  is  relieved  by  stretching  this  tendon.  Pains  in  the 
feet  and  legs  of  various  types  may  be  caused  by  flat-foot  and  this  condi- 
tion should  always  be  carefully  considered. 

Treatment,  medical  or  surgical,  seems  to  do  little  for  the  disorder, 
which  is  very  chronic.  Patients  are  better  in  cold  weather,  and  when 
resting  the  feet.  Leeches,  the  cautery,  the  iodides,  and  broad  shoes 
with  rubber  heels  are  serviceable. 

Coccygodynia  is  a  neuralgia  affecting  the  lower  posterior  branches 
of  the  sacral  nerves.  It  occurs  oftenest  in  women  and  is  caused  by 
casual  injury  and  labor.  Coccygeal  pains  occur  also  in  spinal  irritation 
and  reflexly  from  pelvic  disease.  The  disease  is  a  most  annoying  one, 
as  it  interferes  with  sitting  and  walking.  There  is  often  also  pain  at 
stool,  and  the  parts  are  tender  to  pressure.  The  disease  is  usually 
one  involving  the  fibrous  structures  of  the  coccyx,  and  is  more  an  articular 
and  bony  than  a  nervous  disorder.  Surgical  treatment,  such  as  amputa- 
tion of  the  coccyx,  may  be  needed,  and  is  sometimes  effective,  but  not 
in  the  cases  in  which  there  is  only  a  neurasthenia  with  spinal  irritation, 
for  here  the  trouble  seems  to  be  more  a  habit  pain  or  psychosis. 

PERIPHERAL  VASOMOTOR  AND  TROPHIC  NEUROSES 

Symmetrical    Angio -neurotic     Gangrene,     or    Raynaud's    Disease 

{Abortive  Form  k?iown  as  Digiti  Mortui). — Symmetrical  gangrene  or 
Raynaud's  disease  is  a  rare  affection  characterized  by  spasm  of  the  vessels 
of  the  extremities,  coldness,  pallor,  waxiness  of  fingers  or  toes,  or  by 
blueness,  mottling,  swelling,  and  pain,  followed  often  by  a  dry  gangrene 
of  some  of  the  fingers  or  toes. 

The  name  is  a  poor  one  and  leads  to  confusion.  The  disease  is 
usually  a  peripheral  obliterating  endarteritis,  affecting  oftenest  the 
fingers  and  toes,  but  attacking  at  times  the  nose,  ears  and  even  proximal 
parts  of  the  body,  such  as  the  legs.  It  is  an  evidence  of  many  different 
morbid  conditions.  It  is  seen  in  some  types  of  acute  rheumatism, 
accompanied  perhaps  with  purpura  and  ecchymoses.  It  may  be  a  toxic 
angio-neurosis. 

The  disease  occurs  usually  in  children  and  young  adults.  Women 
are  affected  oftener  than  men.  Anaemia,  chlorosis,  and  neurasthenic 
states  predispose  to  it.  Malarial  infection,  acute  infectious  fevers, 
nephritis,  occupations  that  lead  to  exposure,  such  as  washing,  are  causa- 
tive factors.  Diabetes  and  syphilis  are  also  causes  by  leading  to  vascular 
disease. 

Symptoms. — The  disease  comes  on  rather  suddenly  and  affects 
oftenest  two  or  three  fingers  of  both  hands.     In  its  early  and  mild 


198  DISEASES    OF    THE    NEEVOUS    SYSTEM 

degree  there  are  simply  a  coldness,  numbness  and  waxy  pallor  of  the 
fingers.  The  skin  looks  shrunken.  There  is  slight  anaesthesia.  The 
extremities  feel  as  if  dead.  After  a  few  hours  this  passes  away,  but 
returns  again  and  may  finally  become  an  almost  constant  condition. 
Beginning  in  one  or  two  fingers,  it  may  finally  involve  all.  The  toes,  tip 
of  the  nose  and  ears  may  be  similarly  affected,  though  this  is  rare  in  the 
milder  form.  Exposure  to  cold,  even  slight,  is  the  common  excitant 
of  the  lesser  form  of  the  trouble,  which  is  commonly  known  as  ''digiti 
mortui,"  "dead  fingers,"  or  "local  syncope." 


Fig.  87. — Raynaud's    disease.     {Howard    Fox.) 

In  severer  grades  the  fingers  become  blue,  swollen,  and  there  are 
burning  sensations  and  much  pain,  but  no  ansesthesia.  This  condition 
is  known  as  that  of  "local  asphyxia,"  and  it  is  usually  followed  by 
gangrene. 

In  the  gangrenous  stage  small  blisters  appear  on  the  distal  phalanges, 
which  fill  with  bloody  serum,  then  dry  up,  and  beneath  the  scab  ulcera- 
tion begins,  which  is  shallow  and  soon  heals,  leaving  a  scar.  The  process 
then  stops.  In  very  rare  cases  the  whole  tip  of  the  finger  or  toe,  including 
the  bone,  becomes  involved.  The  process  as  stated  may  attack  the  ears, 
lips,  tongue  and  even  parts  of  the  trunk.  Along  with  this  gangrenous 
process  there  is  often  a  hsematuria. 

The  dead-finger  trouble  may  last  but  a  few  days  or  weeks  or  it  may 


SBNSOEY    NEUROSES    OF    THE    CEREBROSPINAL    NERVES         199 

continue  for  months.  The  gangrenous  stage  lasts  about  three  weeks. 
It  lasts  longer  if  it  comes  on  in  one  finger  after  the  other.  The  disease  is 
one  of  months,  and  it  is  liable  to  recur. 

The  diagnosis  must  be  made  from  senile  gangrene,  frostbite,  ergot 
poisoning  and  alcoholic  neuritis. 

Pathology. — A  neuritis  has  been  found  in  some  cases  of  so-called 
Raynaud's  disease,  but  this  is  secondary.  In  most  cases  there  has  been 
found  an  obliterating  endarteritis  (Jacoby,  Sachs).  The  trouble  is  in 
some  cases  apparently  functional  or  at  least  temporary  and  due  to  the 
combination  of  an  oversensitive  nervous  system  and  some  irritant,  such 
as  impoverished  blood,  malaria,  or  other  toxic  agent,  which  causes 
spasm  and  probably  some  temporary  endarteritis.  In  a  small  per  cent, 
of  cases  the  disease  is  associated  with  scleroderma. 

Prognosis. — The  cases  usually  get  well,  but  the  course  is  long  and 
there  may  be  relapses.  In  only  the  rarest  instances  has  death  occurred, 
and  then  from  a  serious  and  progressive  arterial  disease. 

Treatment. — Galvanism  to  the  spine  and  limbs,  warm  applications, 
anodynes,  tonics,  are  indicated.  Nitroglycerine,  the  iodides,  chloral, 
may  be  tried.  The  frequent  short  application  of  rubber  bandages  giving  a 
kind  of  massage  to  the  vessels  has  been  recommended.  Baking  the  part 
is  sometimes  most  efficacious. 


CHAPTER  XI 
DISEASES  OF  THE  SPINAL  CORD 


Posterior  median_ 
septum 


Cervical  swelling 

Sulcus  inter-. 

medius  posterior 

Posterior  lateral_ 
sulcus 


Lumbar  swelling- 


Fig.  88. — Showing 
the  relative  size  of  the 
different  parts  of  the 
cord.     {Cunningham.) 


ANATOMY  AND  PHYSIOLOGY 

Anatomy. — The  spinal  cord  is  aslender,  cylindrically 
shaped  organ.  It  is  from  42  to  45.7  cm.  (sixteen  and  one- 
half  to  eighteen  inches)  long,  being  shorter  absolutely  and 
relatively  in  women.  Its  weight  is  about  thirty-three  grams 
(one  ounce).  It  is  suspended  in  the  vertebral  canal,  where 
it  reaches  in  all  persons  over  one  year  of  age  as  far  down  as 
the  second  lumbar  vertebra.  In  new-born  infants  it  extends 
to  the  third  lumbar  vertebra. 

It  is  divided  into  cervical,  dorsal  or  thoracic,  lumbar 
and  sacral  portions,  corresponding  with  the  nerves  it  gives 
off.  These  are  respectively  four,  ten  and  one-half,  two,  and 
one  and  one-half  inches  long  (see  Fig.  88).  Its  shape  on 
cross-section  is  nearly  round,  except  in  the  lower  cervical 
region,  where  it  is  flattened  antero-posteriorly.  Its  average 
diameter  is  1  cm.  (two-fifths  of  an  inch).  It  has  two  swell- 
ings or  enlargements,  the  cervical  and  lumbar.  Their  posi- 
tions, size  and  extent  are  shown  on  the  diagram.  Its  specfic 
gravity  is  1.030. 

It  is  surrounded  by  three  membranes,  all  of  which  are 
continuous  with  the  corresponding  envelopes  of  the  brain. 
They  are  the  dura  mater,  the  arachnoid  and  the  pia  mater 
(Fig.  89). 

The  spinal  cord  is  movable  up  and  down  in  its  canal  to  the 
extent  of  from  one-half  to  one  inch. 

The  Nerve-roots. — The  spinal  nerve-roots  are  covered 
with  the  pia  and  arachnoid.  They  pierce  the  dura  in  two 
places  and  unite  to  form  a  mixed  nerve.  The  dura  mater  is 
prolonged  over  the  nerves  as  they  pass  through  it,  forming  a 
tubular  sheath.  The  anterior  roots  are  the  larger.  At  the 
point  of  exit  of  the  nerves  from  the  cord  a  slight  constriction 
is  formed. 

The  Root  Ganglia. — On  each  posterior  root,  outside  the 
dura,  is  a  posterior  spinal  ganglion.  The  ganglia  lie  in  the 
intervertebral  canals,  except  those  on  the  sacral  nerves. 

Fissures. — Throughout  the  whole  length  of  the  cord  there 
are  two  median  fissures,  called  the  anterior  and  posterior. 

Columns. — These  fissures  and  the  lines  formed  by  the  exit 
of  the  roots  divide  the  cord  into  four  columns — anterior,  pos- 
terior and  two  lateral. 

The  Composition  of  the  Cord. — The  Cord  is  composed  of 
white  and  gray  matter.  The  white  matter  lies  outside  and 
is  composed  mainly  of  nerve-fibres,  the  gray  matter  mainly 
of  nerve-cells.     Each  has  also  neuroglia,  connective  tissue, 

200 


DISEASES    OF    THE    SPINAL    CORD 


201 


and    blood-vessels.      In  the  gray  matter  is  a  central  canal  lined  with  epithelial 
cells. 

The  Gray  matter  is  arranged,  as  shown  in  the  figures,  somewhat  in  the  shape  of  a 
letter  H.  Its  different  parts  are  called  the  anterior  and  posterior  horns  and 
intermediate  gray.  At  certain  levels  there  are  lateral  horns.  The  graj''  matter  changes 
in  shape  at  different  levels  of  the  cord.  It  is  greatest  in  amoimt  at  the  lumbosacral 
junction  (23.33  sq.  mm.);  next  at  the  cervical  enlargement  (sixth  cervical)  (17.32  sq. 
mm.).  It  increases  in  amount  relatively  to  the  white  matter  from  above  downward. 
The  gray  matter  of  the  two  halves  of  the  cord  is  connected  by  a  bridge  or  commissure. 
The  anterior  part  is  composed  of  white  meduUated  nerves  and  is  called  the  white 
commissure.     The  posterior  is  composed  of  very  fine  nerve-fibres,  mostly  meduUated 


Fig.  89. — V,  Body  of  vertebra;  V,  spinous  process;  1,  ligament;  2,  vessels;  3.  dura 
mater  with  the  arachnoid  lying  directly  beneath  it;  4,  anterior  root;  5,  posterior  root; 
6,  spinal  ganglion;  7,  ligament. 


collaterals,  called  the  gray  commissure.  Between  the  two  is  the  central  canal,  and 
surrounding  it  is  the  central  gelatinous  substance,  composed  of  neuroglia. 

The  posterior  horns  reach  to  the  periphery.  They  are  divided,  beginning  from 
without,  into  the  rim  zone  or  Lissauer's  column,  the  spongy  zone,  and  the  gelatinous 
substance  of  Rolando.  The  rim  zone  is  composed  of  very  fine  nerve-fibres;  the  spongy 
zone  and  gelatinous  substance  are  composed  of  very  small  nerve-cells,  some  having 
continuous  neuraxons  (cells  of  Deiter)  and  some  having  rapidly  branching  neuraxons 
(cells  of  Golgi).  The  substance  of  Rolando  is  extremely  rich  in  nerve-cells  and  is  not 
made  up  of  neuroglia,  as  was  once  supposed. 

To  sum  up,  we  have  the  gray  matter — 

Arranged  in:  Composed  of: 

anterior,  a.  A  ground  substance  of  neuroglia  and  con- 

1.  Horns  j  lateral,  nective  tissue  forming  the  substantia 

I  posterior.  spongiosa. 


202  DISEASES    OF    THE    NEEVOUS    SYSTEM 

2,  Intermediate  gray.  b.  Cell  groups:  internal,  anterior,  etc. 

c.  Plexuses  of  fine  nerve  fibres,  e.g.,  in  the 

rim  zone. 

d.  Masses  of  neuroglia: 

(1)  The  central  gelatinous  substance. 

(2)  The  periphery  of  the  cord  and  the 
spongy  zone. 

e.  Blood-vessels  and  connective  tissue. 

Now,  taking  up  some  of  these  factors  in  detail,  we  find  that : 

(a)  The  ground  substance  of  the  gray  matter  is  made  up  of  a  fine  mesh-work  of 
fibres  which  are  the  processes  of  neuroglia  cells  and  of  nerve-cells.  Besides  this,  there 
is  some  connective  tissue,  and  there  are  prolongations  from  the  base  of  the  epithelial 
cells  lining  the  central  canal. 

(b)  The  nerve-cells  are,  in  part,  arranged  in  groups  with  the  long  axis  parallel  to 
that  of  the  cord.  The  cells  are  surrounded  by  a  rich  plexus  of  dendrites  and  end 
brushes,  as  well  as  by  the  supporting  neuroglia  matrix,  a  little  connective  tissue,  and 
many  small  blood-vessels.  The  cell  groups  are  named  in  accordance  with  their  posi- 
tion— internal,  antero-lateral,  lateral  median,  posterior  or  sensory  cells,  and  the  cells 
of  Clark's  column  (Fig.  90). 

This  nomenclature  answers  for  ordinary  anatomical  descriptions.  Histologically, 
we  find  two  kinds  of  cells,  the  root  cells  and  column  or  tract  cells  (Strangzellen).  The 
former  are  cells  whose  neuraxons  pass  out  to  form  the  anterior  roots.  They  form  the 
great  part  of  the  anterior  horns.  Deep  in  the  anterior  horns  are  a  few  root  cells,  whose 
neuraxons  pass  into  the  posterior  roots  and  hence  to  the  ganglionic  system.  The  col- 
umn cells  are  found  in  the  posterior  horns,  intermediate  gray  and  to  some  extent  in  the 
anterior  horns.  Their  neuraxons  pass  to  the  white  matter  of  the  same  or  opposite 
side,  and  furnish  commissural,  associative  and  even  long  column  fibres. 

The  anterior-horn  root  cells  are  arranged  in  groups,  which  overlap  each  other. 
Each  group  has  the  special  duty  of  presiding  over  certain  sets  of  muscles  or  other  organs 
which  have  a  common  function.  These  cells  are  large  in  size,  35  to  100  n  Moo  to  Mso 
in.);  they  are  multipolar,  having  five  or  six  processes,  one  of  which  is  an  axis-cylinder 
process,  which,  in  lower  animals  at  least,  gives  off  a  collateral  before  it  leaves  the  cord. 
The  cells  in  the  central  parts  of  the  horn  are  the  smaller;  the  cells  in  the  lumbar  swell- 
ing are  largest,  because  they  are  connected  with  long  nerves.  The  cells  of  the  cervical 
swelling  are  next  in  size.  The  cells  of  the  posterior  horn  are  small  and  multipolar. 
The  cells  of  Clark's  column  are  bipolar,  30  to  60  ju  (^-^oo  to  J4oo  in.)  in  diameter, 
and  are  arranged  with  their  long  diameter  parallel  to  the  axis  of  the  cord.  They  are 
grouped  together  in  a  kind  of  nest  at  the  inner  and  central  part  of  the  posterior  horn 
(see  Fig.  90).  Clark's  column  is  most  distinct  from  the  eighth  dorsal  to  the  second 
lumbar  nerves,  but  extends  up  as  far  as  the  last  cervical.  An  analogous  group  of  cells 
is  found  at  the  level  of  the  second  and  third  sacral  nerves.  A  small  group  of  spindle- 
haped  cells  lies  in  the  intermediate  gray  matter  at  the  base  of  the  posterior  horns. 
There  are  other  minor  groups  of  cells  which  it  is  not  necessary  to  describe  here. 

The  white  matter  of  the  cord  is  composed  mainly  of  neuraxons  and  the  collaterals  of 
these  running  in  a  supporting  network  of  neuroglia,  connective  tissue  and  blood- 
vessels. Surrounding  it  and  lying  just  beneath  the  pia  mater,  is  a  thin  layer  of  neurog- 
lia 5  to  50;u  (J^soo  to  }io  in.)  thick.  The  neuraxons  are  meduUated  but  have  no 
neurilemma,  and  but  few,  if  any,  nodes  of  Ranvier.  There  are  two  kinds:  the  large 
(81  to  20ai)  and  the  small  (2  to  3^)  in  diameter.  The  small  fibres  make  up  the  postero- 
internal (GoU's)  column  entirely,  and  are  numerous  in  the  deep  part  of  the  lateral 
columns,  but  they  are  found  in  all  regions.  The  fibres  run  up  and  down  for  the  most 
part,  but  constantly  send  off  branches  to  the  gray  matter.     They  are  arranged  in  col- 


DISEASES    OF    THE    SPINAL    CORD 


203 


umns,  the  division  being  based  partly  on  anatomical,  partly  on  physiological,  and 
partly  on  embryological  grounds. 

Anatomically,  there  is  a  simple  and  natural  division,  which  we  have  already  given, 
into  the  anterior,  lateral  and  posterior  columns,  the  divisions  being  made  by  the  median 
fissures  and  the  roots  of  the  nerves. 

On  physiological  and  embryological  grounds  the  columns  are  further  subdivided  as 
follows : 


The    anterior    columns 
are    divided  into 


r  Direct  pyramidal  tract. 

\  Anterior  fundamental  column. 


The  lateral  columns  are  di 
vided  into 


'  Lateral  fundamental  column. 
Lateral  limiting  layer. 
Crossed  pyramidal  tract. 
Direct  cerebellar  tract. 
A  ventral  cerebellar  tract,  or  Gowers'  tract. 

In  the  anterior  and  lateral  r  Rubro-spinal  tract, 
columns      the     principal  \  Vestibulo-spinal  tract, 
tracts  are :  I  Tecto-spinal  tract. 

Postero-internal  column,  or  column  of  Goll. 


The  posterior  columns  ai-e 
divided  into 


Postero-external  columns, 
or  column  of  Burdach. 


Burdach's  column  is  di- 
vided into 
Middle  root  zone. 
Posterior  root  zone. 


The  ventral  zone. 
The  comma. 
The  oval  zone. 
The  triangular  column. 
.  Rim  zone,  or  column  of  Lissauer. 

The  fibres  which  make  up  these  columns  are  of  two  kinds — long  or  projection,  short 
or  associative. 

The  long  fibres  connect  the  different  levels  of  the  cord  with  the  brain,  and  the 
posterior  spinal  ganglia  with  nuclei  in  the  upper  part  of  the  cord. 

The  short  or  associative  fibres  connect  different  levels  of  the  cord  with  each  other, 
and  also  connect  the  two  halves  of  the  cord  at  the  same  levels.  The  long-fibre  tracts 
lie  on  the  periphery  of  the  cord,  as  a  rule;  the  short- fibre  tracts  lie  near  the  central  gray. 

The  names  of  the  long-fibre  tracts  are  the  direct  and  crossed  pyramidal,  the  direct 
cerebellar,  the  antero-lateral  ascending,  or  ventral  cerebellar,  the  rubro-,  vestibulo-, 
and  tecto-spinal  tracts,  the  postero-internal  or  column  of  Goll  and  the  upper  part  of 
the  column  of  Burdach. 

The  direct  pyramidal  tract  lies  along  the  anterior  median  fissure  and  extends  down  as 
far  as  the  lower  part  of  the  dorsal  cord.  Its  fibres  cross  over  in  the  anterior  commis- 
sure at  various  levels  and  connect  with  the  cells  of  the  anterior  horns. 

The  crossed  pyramidal  tract  extends  down  the  whole  length  of  the  lateral  column  of 
the  cord  and  sends  its  fibres  to  the  anterior  horns  of  the  same  side. 

Both  of  the  above  tracts  are  continuations  of  the  anterior  pyramids  or  motor  tracts 
of  the  medulla.  These  pyramids  divide  at  the  lower  end  of  the  medulla,  about  90 
per  cent,  of  fibres  crossing  over  to  form  the  crossed  pyramidal  tract  and  10  per  cent, 
continuing  on  the  same  side.  Some  of  the  fibres  of  the  crossed  pyramid  redecussate 
(in  lower  animals)  and  enter  the  pyramidal  tract  of  the  side  on  which  they  started. 

The  extra-pyramidal  tracts,  are  tracts  of  efferent  fibres  which  have  to  do  with  mo- 
tion, tonus,  and  the  higher  automatic  actions. 


204 


DISEASES    OF   THE    NERVOUS   SYSTEM 


Cortico-spinal  (pyramidal)  tract 


Rubro-spinal  tract 


Tecto-spinal  tract 


Vestibulo-spinal  tract 


Olivo-spinal  (triangular)  and  ponto- 
spinal  tracts 


■  Motor  and  inhibition 

Automatic,  higher  reflexes, 
and  synergy 

Automatic,  higher  reflexes, 
and  synergy 

Automatic,  higher  reflexes, 

■  and  synergy 

Automatic,  higher  reflexes, 

■  and  synergy 


THE  PYRAMIDAL  AND  EXTRA-PYRAMIDAL  TRACTS :  LONG 
EFFERENT  TRACTS  BETWEEN  BRAIN  AND  SPINAL  CORD 

Spino-tectal   tract 


Spino-thalamic  tracts 


Ventral  cerebellar  (Gowers')  tract 


Reflex 

Cutaneous  sensations  and 

higher  reflexes 

Visceral  and  equilibrium 

Visceral  and  equilibrium 

Musculo-articular  and  cuta- 
neous  sensations 

The  Long  Afferent  Tracts  Between  the  Brain  and  the  Spinal  Cord. 


Direct  cerebellar  tract 


Posterior  column  tracts  (Goll  and  Burdach) 


Antero-lateral  fundamental  column 


Posterior  fundamental  column  (fasciculus  proprius) 


Postero-median  tract  (descending)  including: 


Postero-lateral  tract   (descending) 


The  comma  tract 
I      Oval  tract 
j      Septo-marginal  tract 

Median  triangular  tract 


Marginal  tract  (Lissauer's) 


Ventral  commissural  tract 


The  Short  or  Association  Tracts  of  the  Spinal  Cord. 


DISEASES    OF   THE    SPINAL    CORD 


205 


Sixth  Cervical  Segment. 


First  Liimbar. 


Jt'jj.  JojT'. 


7<^s?'j^coI 


>. 


.>^ 


J       y 


A 


First  DorsaL 


^-  7'oi7:^oof. 


"In^Jicot. 


M 


Fourtli  SacraL 


•/?./ 


/ 


Jh^tTluoT. 


-  --;^/i'/ ;?Qaf- 


Eighth  Dorsal. 


First  Sacral. 


Fig.  90. — Showing  the  arrangement  of  the  gray  and  the  white  matter  at  different 
levels  of  the  cord,  also  the  columns  and  cell  groups. 


206 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


The  direct  cerebellar  tract  begins  at  the  level  of  the  first  lumbar  nerve.  Its  fibres 
originate  in  the  vesicular  column  of  Clark.  They  pass  up  to  the  cerebellum  and  go 
chiefly  to  the  cortex  of  the  vermis  without  crossing. 

Th.e\entral  cerebellar  tract,  or  column  of  Gowers,  extends  nearly  the  whole  length 
of  the  cord.  Its  fibres  come  from  the  anterior  commissure  and  the  sensory  cells  of  the 
opposite  posterior  cornu.  They  pass  through  the  medulla  and  pons,  turn  and  enter 
the  cerebellum  to  end  in  the  cortex  of  the  vermis.  A  few  fibres  pass  directly  to  the 
optic  thalamus. 

The  rubrospinal  tract  originates  in  the  red  nucleus;  it  crosses  to  the  opposite  side, 
passes  down  through  the  pons  and  medulla,  runs  in  the  lateral  column  of  the  cord 
forming  a  triangular  or  wedge-shaped  tract  along  the  anterior  or  ventral  part  of  the 


Olive  bundle 
Goll's  column. 
Comma  bundle 
Burdach's  column 
Root-zone 
Lissauer's  zone. 


Septo-marginal . 


Dorsal  spino- 
cerebellar tract 
(Fleschsig). 


Lateral  pyram- 
idal tract. 


Area  of  rubi  o- 
spinal  trac  t 
Ventral  spino- 
cerebellar tr 
(Gower's). 
Spino-thalanuc 
tr. 

Vestibulo- 
spinal tra(  t 

Lateral  funda- 
mental column 


Spino-olivary  tract' 
(Helwig) . 


tecto-spinal  tract.  |  tecto-spinal  tr. 

direct  pyramidal  tract. 

Fig.  91. — Showing  the  tracts  and  columns  of  the  spinal  cord.  Descending  tracts 
are  in  red;  ascending  in  green.  The  vestibulo-spinal  is  not  as  extensive  as  indicated 
and  lies  mainly  in  the  ventral  column.  The  rubro-spinal  tract  is  not  as  sharply  de- 
fined as  indicated. 

crossed  pyramid  tract.  It  extends  as  far  down  as  the  sacral  cord.  Its  fibres  end  in 
the  anterior  horns. 

The  vestibulo-spinal  tract  arises  in  Deiter's  nucleus,  crosses  and  runs  in  the  lateral 
column  of  the  cord  in  front  of  the  rubro-spinal.  It  may  extend  to  the  anterior  column. 
It  passes  down  as  far  as  the  lumbar  cord.     Its  fibres  end  in  the  anterior  horns. 

The  tecto-spinal  tract  originates  in  the  corpora-quadrigemina  and  takes  a  similar 
course  to  the  preceding  tract,  a  median  part  running  in  the  anterior  and  a  lateral 
in  the  lateral  columns. 

Several  other  tracts  are  described.  These  together  with  the  above  three  small 
tracts  degenerate  downward  and  are  spoken  of  collectively  as  the  extra-pyramidal 
tracts.  , 


DISEASES    OF   THE    SPINAL   CORD 


207 


The  posterior  columns  are  made  up  of  fibres  that  come  from  the  posterior  spinal 
ganglion  and  pass  directly  into  the  posterior  columns,  then  ascend  to  nuclei  near  the 
medulla  where  they  end.  These  fibres  are  called  exogenous.  The  columns  also  re- 
ceive some  fibres  from  the  tract  cells  in  the  posterior  horns;  and  they  are  called  endoge- 
nous fibres. 

The  exogenous  fibres  in  the  sacral  lumbar  and  lower  dorsal  cord  pass  inward  and 
form  the  postero-internal  column  or  GoU's  column.  This  is  then  small  below  and 
larger  in  the  cervical  region.     They  end  in  the  nucleus  of  GoU's  column  (nucleus  gracilis). 

The  exogenous  fibres  in  the  upper  part  of  the  cord  pass  up,  tying  to  the  outer  side 
of  the  column  of  Goll.  They  form  the  column  of  Burdach  and  end  in  the  nucleus  of 
Burdach  (nucleus  cuneiformis). 


Fig.  92 


I.  Showing  the  connections  of  the  anterior  and  posterior  roots  and  cornua  with  each 
other  (Cajal).     A,  anterior  root;  B,  posterior  root;  a,  collaterals;  d,  end-brushes. 

II.  Showing  the  association  or  short-fibre  system  of  the  cord  (Cajal).  a,  anterior 
cornua  cell;  b,  c,  d,  association  fibres;  e,  posterior  association  fibres. 

The  column  of  Burdach  is  thus  not  distinctly  formed  as  a  long  fibre  tract  except  in 
the  upper  part  of  the  cord. 

The  names  of  the  short-fibre  columns  are  the  anterior  and  the  lateral  fundamental 
columns,  the  lateral  limiting  layer  and  the  lower  part  of  the  column  of  Burdach. 

The  posterior  columns  also  contain  three  short-fibre  columns  whose  cells  of  origin 
lie  in  the  gray  matter  of  the  cord.  The  fibres  in  the  cervical  region  lie  in  the  shape  of  a 
comma  (comma  of  Schultze),  in  the  lumbar  region  in  the  shape  of  an  oval  (oval  zone  of 
riechsig),  in  the  sacral  zone  in  the  shape  of  a  triangle  (triangle  of  Gombault).  Besides 
this  there  is  a  zone  of  short  fibres  lying  close  to  the  gray  commissure  the  whole  length 
of  the  cord — ventral  zone  or  posterior  fundamental  column. 


208  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  Relations  of  the  Different  Parts  of  the  Spinal  Cord  to  the  Peripheral  Nerves, 
and  with  Each  Other. — I  will  begin  with  a  description  of  the  way  in  which  the  anterior 
and  posterior  nerve-roots  are  conected  to  the  cord;  then  describe  the  mode  in  which  the 
different  columns  and  cell  groups  are  connected  with  each  other;  and  finally  I  will 
indicate  briefly  the  connections  of  the  cord  with  the  brain. 

The  anterior  nerve-roots  are  connected  directly  with  the  anterior-horn  cells,  of  which 
they  are  processes,  and  together  with  which  they  form  the  peripheral  motor  neurons. 
It  is  possible  that  in  man  they  send  off  collaterals  before  leaving  the  cord. 

The  cells  of  the  anterior  horn  are  surrounded  by  two  chief  sets  of  "end  brushes," 
one  coming  from  the  pyramidal  and  other  descending  tracts,  the  other  from  the  pos- 
terior horns  and  roots.  Thus  these  cells  are  in  relation  with  impulses  from  the  brain 
and  from  the  periphery. 

The  posterior  nerve-roots  originate  in  the  cells  of  the  spinal  ganglia.  These  give  an 
axon  which  divides  and  sends  off  a  peripheral  branch  to  form  the  sensory  nerve,  and  a 
central  branch  which  passes  into  the  .spinal  cord  forming  the  posterior  root.  On 
entering  the  cord  the  fibres  of  the  posterior  root  divide  like  a  T  and  pass  up  for 
one  or  more  inches  and  down  for  a  short  distance  only.  These  root-fibres,  with  their 
cells  of  origin  and  the  sensory  nerve-fibres,  form  together  the  peripheral  sensory  neurons. 

The  peripheral  sensory  neurons  send  their  axons  into  the  spinal  cord  through  the 
posterior  roots,  and  these  axons  divide,  run  up  and  down  the  cord  for  a  short  or  long 
distance  and  then  end  in  terminal  arborizations  about  different  groups  of  cells. 

1.  Some  pass  directly  into  the  columns  of  Goll  or  Burdach  on  the  same  side  and 
pass  up  to  end  in  the  nuclei  of  these  columns. 

2.  Some  pass  to  cells  in  the  posterior  horns  of  both  sides  and  there  end. 

3.  Some  pass  to  cells  of  the  column  of  Clark  of  the  same  side. 

4.  Some  pass  to  cells  of  the  anterior  horns  of  both  sides. ^ 

1  There  are,  according  to  Ingbert,  about  650,000  sensory  fibres  in  the  posterior 
spinal  roots;  each  cutaneous  fibre  supplies  from  1  to  3  sq.  mm.  of  surface. 

The  different  parts  of  the  spinal  cord  are  connected  by  the  short  fibres  which  unite 
different  levels  of  the  cord,  and  by  commissural  fibres  which  unite  the  different  halves 
of  the  cord.  These  short  and  commissural  fibres  originate  in  groups  of  nerve-cells 
lying  in  the  central  parts  of  the  gray  matter  and  which  we  have  called  column  nerve- 
cells.  They  are  small  and  multipolar.  Some  are  distributed  sparsely  in  the  white 
columns.  Fibres  arise  from  them,  run  in  the  commissures  and  short-fibre  tracts,  and 
end  in  brushes  which  put  the  fibres  in  relation  with  various  cell  groups. 

DIAGNOSTIC  PHYSIOLOGY 

General. — The  spinal  cord  is  made  up  of  (1)  peripheral  motor  and  sensory  neurons; 
(2)  the  upper  or  encephalo-spinal  neurons;  (3)  short  associative  neurons.  Lesions 
of  the  peripheral  motor  neuron  cause  motor  irritation  or  a  severe,  flaccid  paralysis 
and  atrophy.  Lesions  of  the  peripheral  sensory  neurons  cause  pain,  paraesthesia, 
ataxia  and  anaesthesia  and  secondary  trophic  troubles.  Lesions  of  the  upper  or 
cerebrospinal  neurons  cause  a  spastic  paralysis  without  atrophy.  Lesions  of  the 
secondary  sensory  neurons  cause  little  pain  or  sensory  irritation,  but  lead  to  anaesthesia 
paraesthesia,  ataxia,  etc. 

The  relations  of  the  spinal  cord  to  the  brain  will  be  described  in  connection  with 
the  anatomy  of  the  brain. 

Peripheral  Palsies ;  Radicular  or  Root  Palsies ;  Nuclear  Palsies. — If  the  nuclear 
groups  of  motor  cells  in  a  single  segment  of  the  spinal  cord  are  destroyed,  e.g.  the 
fifth  cervical  segment,  we  get  a  partial  paralysis  of  the  muscles  supplied  from  this 
segment,  because  these  nuclear  groups  overlap  and  are  not  each  assigned  to  a  single 
segment. 


DISEASES    OF    THE    SPINAL    CORD 


209 


If  an  anterior  root  is  cut  across,  we  also  get  a  partial  paralysis,  because  muscles 
generally  are  supplied  from  several  different  roots  as  well  as  from  several  different 
segments.  Hence  a  single  segment  or  root  palsy  is  rarely  a  complete  one.  On  the 
other  hand,  a  section  of  a  motor  nerve  may  cause  a  complete  paralysis  of  a  muscle 
or  group  of  muscles.     Hence  a  ■peripheral  palsy  may  be  complete. 

If  the  entire  nuclear  group  of  cells  controlling  a  muscle-group  is  destroyed,  as 
happens  in  anterior  poliomyelitis,  we  also  get  a  complete  paralysis — nuclear  palsy. 

Sensory  Ansaethesia  from  Peripheral, 
and  Radicular  Lesion. — In  the  same  way 
we  get  peripheral  anesthesia  over  a  def- 
inite cutaneous  area  when  a  peripheral 
sensory  nerve  is  cut. 

When  one  posterior  root  is  cut  we  got 
no  anaesthesia;  when,  however,  two  or 
more  are  cut  we  get  bands  of  anaesthesia 
known  as  radicular  or  segmental  zones. 
These  have  been  determined  by  animal 
experiment  and  operations  and  disease, 
so  that  we  have  charts  showing  the  radic- 
ular zones  produced  by  cutting  two  pos- 
terior roots  at  different  levels.  They 
are  marked  singly  for  purposes  of  con- 
venience, only  (see  Figs.  27  and  28). 

Automatic  Centres. — The  nerves  and 
cells  of  the  cord  are  arranged  in  com- 
plex groups  which  preside  over  certain 
functions  or  respond  in  a  definite  wa:y  to 
certain  stimuli.  These  are  called  the 
spinal  automatic  centres..  They  are  the 
cilio-spinal,  secretory,  vasomotor,  genital, 
vesical  and  rectal.'  The  important  parts 
of  these  centres  lie  deep  in  the  gray 
matter  on  either  side  of  the  central  canal, 
but  nearer  the  base  of  the  posterior  horns. 
Lesions  of  the  white  matter  or  of  the  an- 
terior or  posterior  horns  do  not  directly 
affect  them. 

The  cilio-spinal  centre  lies  in  the  eighth 
cervical  and  the  first  dorsal  segment.  Its 
stimulation  causes  the  pupils  to  dilate. 

The  genital  centres,  including  those  for 
erection  and  ejaculation,  reach  from  the 
first  to  the  third  sacral  segment,  inclusive. 

The  bladder  and  rectal  centres  are  in  the 
fourth  and  fifth  sacral  segments,  extend- 
ing up  and  down  a  short  distance,  the  bladder  being  perhaps  a  little  lower. 

The  spinal  vasomotor  centres  extend  from  the  second  dorsal  to  the  second  lumbar 
segments.  The  vasodilator  nerves  pass  out  by  the  anterior,  the  constrictor  by  the 
posterior  root  (Gaskill). 

The  cells  of  the  posterior  horns  are  sensory  in  function  and  are  connected  with  the 
tactile,  pain,  temperature  and  reflex  fibres  of  the  posterior  roots. 
14 


Fig.  93. — Showing  the  relation  of  the 
spinous  processes  to  the  points  of  origin 
in  the  cord  of  the  spinal  nerves.  The 
nerves  are  shown  in  black  lines  as  they 
come  from  the  spinal  canal.  The  dotted 
lines  show  the  level  at  which  each  nerve 
arises  m  the  cord. 


210 


DISEASES    OF    THE    NERVOUS    SYSTEM 


Topography  and  Localization. — The  neurologist  and  surgeon  need  to  know,  for 
purposes  of  diagnosis: 

1.  The  relation  of  the  spinal  nerve-roots,  at  their  point  of  origin,  to  the  spinous 
processes.  This  is  shown  in  Fig.  93.  In  general  it  will  be  seen  that  the  different 
pairs  of  nerve-roots  arise  opposite  the  spinous  process  of  a  vertebra  one  or  two  seg- 
ments above  those  between  which  it  makes  its  exit.  Thus  the  sixth  cervical  originates 
opposite  the  fourth  cervical  spine,  the  sixth  dorsal  between  the  third  and  fourth 
dorsal  spines,  the  first  lumbar  between  the  eleventh  and  twelfth  dorsal  spines.  There 
is  considerable  variation  in  these  relations. 

2.  The  next  point  desired  is  the  special  function  of  each  pair  of  nerve-roots 
anterior  and  posterior,  and  the  level  of  the  various  centres  in  the  cord.  This  is  shown 
in  the  following  table,  based  on  that  originally  devised  by  Starr,  modified  by  Mills, 
Sachs  and  myself  from  personal  experiments  and  the  clinical  and  pathological  ob- 
servations of  Thorburn  and  others.       (See  Appendix.) 

The  blood-supply  of  the  spinal  cord  is  a  subject  of  great  practical  importance;  and  I 
shall  present  the  matter  here  in  some  detail. 

The  spinal  cord  is  supplied  with  blood  by  branches  from  the  vertebral,  ascending 
cervical  and  superior  intercostal  arteries  above,  and  by  the  dorsal  intercostal,  lumbar 
and  sacral  arteries  below.  These  send  off  small  branches  which  enter  the  spinal  canal 
through  the  foramen  magnum  above  and  the  intervertebral  foramina  at  the  sides: 
they  pierce  the  dura  mater  and  are  distributed  on  the  pia  mater  and  in  the  cord. 
The  arteries  that  thus  supply  the  cord  are  these : 


Primary  Arteries 


Origin  from 


Ending  in 


Anterior  spinal . .  . 

Vertebral  (from  subclav.) 

Anterior  median  spinal  artery. 

Posterior  spinal .  . 

Vertebral. 

Lateral  spinal .... 

Vertebral. 

Lateral  spinal .... 

Ascending   cervical    (from   sub- 

Anterior   and    posterior 

spinal 

clav.). 

root  arteries. 

Lateral  spinal.  .  .  . 

Superior  intercostal   (from  sub- 

Anterior   and    posterior 

spinal 

clav.). 

root  arteries. 

Lateral  spinal .... 

Thoracic       intercostal        (from 

Anterior    and    posterior 

spinal 

aorta). 

root  arteries. 

Lateral  spinal .... 

Lumbar  (aorta). 

Anterior    and    posterior 

spinal 

Lateral  sacral  (from  int.  iliac). 

root  arteries. 

The  anterior  spinal  arteries  are  branches  of  the  vertebrals.  They  unite  to  form 
the  anterior  median  artery,  which  runs  down  the  whole  length  of  the  cord,  receiving 
re-enforcements  from  the  lateral  arteries  (Fig.  94).  The  anterior  spinal  arteries 
themselves  nourish  only  a  few  upper  segments  of  the  cord.  The  anterior  median 
artery  is  not,  as  has  been  taught,  a  true  prolongation  of  the  anterior  spinals,  but  is 
really  made  up  by  the  lateral  spinals.  In  other  words,  the  vertebral  artery  through 
its  branches  nourishes  only  the  upper  cervical  region  of  the  cord.  The  posterior 
spinal  arteries  are  smaller  than  the  anterior  and  unite  on  the  posterior  surface  of  the 
cord.  They  do  not  continue  down  as  a  posterior  median  artery — ^there  is  no  such 
artery;  but  they  help  to  form  two  plexuses  on  the  postero-lateral  surfaces  of  the  cord. 

The  lateral  spinal  arteries  are  derived  from  branches  of  the  subclavian  artery  as 
far  down  as  the  second  dorsal  root;  below  this  point  by  the  thoracic  and  abdominal 
aorta  and  the  internal  iliac.     It  is  an  interesting  fact  that  at  or  a  little  below  the  point 


DISEASES    OF   THE    SPINAL    CORD 


211 


where  the  blood-supply  changes  from  the  subclavian  above  the  heart  to  the  aorta 
below,  pathological  disturbances  frequently  occur  (transverse  myelitis). 


"^^ 


^J'k 


^^^  , 

'^.:^ 


sl^- 


Fig.  94. — The  spinal  cord,  anterior  surface,  showing  the  nerve  roots,  root  arteries, 
and  anterior  plexus.    (Kadyi.) 

Root  Arteries. — The  lateral  spinal  arteries,  after  they  enter  the  spinal  canal,  are 
called  the  root  arteries.  They  pierce  the  dura  mater  and  pass,  some  along  the 
posterior  and  some  along  the  anterior  roots,  to  the  cord.     There  are  about  eight 


212 


DISEASES    OF    THE    NEEVOTJS    SYSTEM 


anterior-root  arteries  (five  to  ten)  and  about  sixteen  posterior-root  arteries  (see  Figs. 
94,  95).  The  anterior  arteries  are  twice  as  large  (1  mm.  in  diameter)  and 
one-half  as  numerous  as  the  posterior.  The  root  arteries  of  the  cervical  region  are 
rather  the  more  numerous.  There  is  a  large  and  constant  anterior-root  artery  in  the 
dorso-lumbar  region.  The  last  two  lumbar,  the  five  sacral  nerves  and  the  unpaired 
coccygeal  nerve  when  it  exists,  are  accompanied  by  small  root  arteries  which  do  not 
reach  up  to  the  cord  itself.  The  lower  part  of  the  spinal  cord  is  supplied  by  large 
root  arteries  from  the  lateral  spinal  arteries.  Hence,  the  theory  of  Moxon  that  the 
circulation  here  is  feeble  is  not  supported  by  Kadyi's  investigations. 

The  Plexuses. — The  anterior  root  arteries  pass  to  the  anterior  median  fissure,  and 
then  divide,  partly  to  form  the  anterior  median  artery  and  partly  to  form  a  rich  plexus 
between  the  anterior  roots;  this  is  called  the  anterior  arterial  plexus .  The  posterior 
root  arteries  subdivide  before  they  reach  the  cord,  and  send  twigs  to  its  lateral  and 


^       B 

Fig.  95. — -The  arterial  supply.  A,  The  artery  of  the  posterior  fissure;  B,  the 
interfunicular;  C,  artery  of  posterior  horn;  D,  of  posterior  root;  E,  of  postero-lateral 
column. 


posterior  surfaces  which  form  the  postero-lateral  arterial  plexus.  The  posterior-root 
arteries  do  not  anastomose  to  any  extent  with  each  other  or  form  a  posterior  spinal 
artery,  as  is  done  by  the  anterior-root  arteries.  There  are,  therefore,  three  relatively 
independent  arterial  plexuses :  the  anterior  plexus,  the  two  postero-lateral  plexuses. 

Veins. — The  veins  of  the  spinal  canal  outside  the  dura  mater  have  valves,  those 
within  it  have  none.  The  veins  reach  the  pia  mater  and  cord  by  passing  along  the 
nerve-roots.  Hence,  we  have  anterior  and  posterior  root  veins,  corresponding  to  the 
root  arteries,  but  more  numerous,  there  being  a  total  of  forty  or  fifty.  The  anterior- 
root  veins  are  more  numerous  than  the  posterior,  but  smaller  (twenty  five  to  tweiity). 
The  veins  are  a  little  larger  than  the  arteries,  the  anterior  veins  being  3^^  to  1  mm., 
the  posterior  IJ^  to  2  mm.,  in  diameter. 

Thus  we  see  that  the  posterior  surface  of  the  cord  has  more  and  smaller  arteries, 
fewer  but  larger  veins.     The  posterior  surface  is  on  the  whole  more  richly  supplied 


5  to  10 

1      mm 

25  to  30 

3-2  to  1      mm 

16 

3^^  mm 

20  to  25 

\}y-2  to  2      mm 

DISEASES    OF    THE    SPINAL    CORD  213 

with  veins,  the  anterior  surface  with  arteries.     The  lateral  surfaces  are  the  least 
vascular. 

Anterior  root  arteries 

Anterior  root  veins 

Posterior  root  arteries 

Posterior  root  veins 

Vessels  of  the  Cord  Substance. — The  cord  is  supplied  by  (1)  central  arteries  which 
are  branches  of  the  anterior  median,  and  by  (2)  peripheral  arteries  which  come  from 
the  plexuses  on  the  pia  mater.  These  two  systems  have  been  called  also  the  centrif- 
ugal and  centripetal,  respectively.  They  are  not  absolutely  independent,  but  are  in 
a  good  measure  so.  The  central  arteries  nourish  chiefly  the  gray  matter,  the  per- 
ipheral arteries  the  white.  Both  systems  are  made  up  of  "end  arteries;"  i.e.,  they  do 
not  anastomose  with  each  other.  Neither  the  central  nor  the  peripheral  arteries  are 
distributed  in  accordance  with  anatomical  relations  or  physiological  functions.  Each 
cell  group,  for  example,  has  a  vascular  supply  from  several  sources. 

The  central  arteries  are  given  off  from  the  branches  of  the  anterior  median  at  the 
bottom  of  the  median  fissure  and  number  about  two  hundred,  each  spinal  segment 
having  six  or  seven.  The  accompanying  central  veins  are  small  and  their  total 
capacity  is  less  than  that  of  the  arteries,  so  that  the  central  arterial  pressure  must  be 
high,  on  account  of  the  poor  venous  outlet  (Kadyi).  Some  of  the  blood  escapes  by 
the  peripheral  veins. 

The  peripheral  arteries  pass  into  the  spinal  cord  for  the  most  part  along  the 
various  connective-tissue  septa.  There  they  branch  and  supply  chiefly  the  white 
matter.  They  supply  the  apex  and  some  of  the  deeper  substance  of  the  posterior 
horns  and  Clark's  columns.  The  arteries  of  the  posterior  septum  are  the  largest  and 
most  numerous,  often  reaching  to  the  gray  commissure.  The  peripheral  arteries  are 
smaller  than  the  corresponding  veins  (0.04  to  0.2  mm.).  The  relation  is  just  the 
reverse,  therefore,  to  that  of  the  central  arteries  and  veins.  The  peripheral  arteries 
are  small,  and  after  passing  into  the  cord  branch  into  minute  vessels  which  pass  up 
and  down  and  soon  become  capillaries.  The  central  arteries,  on  the  other  hand, 
continue  large,  and  run  up  and  down  some  distance  before  they  are  subdivided  into 
capillaries. 

To  sum  up:  The  arteries  predominate  in  total  capacity  in  the  anterior  plexus 
and  central  arteries;  the  veins  in  the  posterior  plexuses  and  peripheral  vessels.  The 
central  arteries  are  larger  and  longer  than  the  peripheral.  Hence  the  blood  circulates 
more  quickly  and  under  greater  pressure  in  the  central  gray  of  the  cord.  Conditions 
of  enfeebled  circulation  would  affect  the  posterior  columns  and  roots  more  than  the 
anterior  and  central  parts  of  the  cord. 


CHAPTER  XII 
THE  DISEASES  OF  THE  SPINAL  CORD 

There  are  about  thirty  diseases  which  may  be  classified  as  belonging 
to  the  spinal  cord.  Most  of  these  are  organic  in  character  and  come  under 
the  head  of  inflammatory  and  degenerative  or  system  diseases.  Func- 
tional disorders  referable  to  the  cord  alone  are  rare;  while  of  organic 
diseases,  those  that  result  from  injury,  syphilis  and  inflammation  are 
the  most  common. 

The  special  diseases  of  the  spinal  cord  are  the  following: 

1.  Malformations. — Myelocele,  meningo-mylocele  (spina  bifida),  men- 
ingocele, heteropia,  amyelia,  micromyelia,  macromyelia,  double  cord. 

2.  Vascular  Disorders. — Anaemia,  hypersemia,  hemorrhage,  endarter- 
itis with  aneurism,  embolism  or  thrombosis,  oedema.  Secondary  to 
these  conditions  are  softenings  and  sclerosis. 

3.  Inflammations. — Meningitis,  myelitis,  multiple  sclerosis.  Second- 
arily, softenings,  sclerosis. 

4.  Degenerations  or  Parenchymatous  Inflammations. — Primary:  pos- 
terior and  combined  scleroses,  hereditary  scleroses,  progressive  muscular 
atrophy  and  allied  types. 

5.  Tuberculosis.- — Miliary,  solitary,  and  meningeal,  causing  2,  3,  7. 

6.  Syphilis. — Which  may  cause  1,  2,  3,  4  and  7. 

7.  Tumors. 

8.  Functional   and   toxic   disorders. 

MALFORMATIONS 

Spina  Bifida  (Rhachischisis  Posterior) 

Spina  bifida  is  a  congenital  hernia  of  the  spinal  membranes,  and 
sometimes  of  the  cord,  through  a  cleft  in  the  vertebra  caused  by  absence 
of  the  vertebral  arches.  It  is  often  really  a  malformation  of  the  vertebral 
canal  rather  than  of  the  cord,  though  both  conditions  may  be  present. 

Etiology. — The  condition  is  not  very  rare,  about  one  child  in  1,200 
(French  statistics)  being  affected.  It  is  often  associated  with  hydro- 
cephalus or  with  some  other  defect  in  development,  such  as  ventral  hernia, 
imperforate  anus  or  pharynx.  Hereditary  influence  is  sometimes  a  factor. 
It  is  a  true  developmental  defect,  and  is  not  due  to  a  primary  dropsy  of 
the  cord,  as  was  once  taught.     It  occurs  rather  oftener  in  females. 

214 


DISEASES    OF    THE    SPINAL    CORD 


215 


Forms. — There  are  three  varieties  described : 

1.  Spinal  meningocele  is  a  condition  in  which  the  spinal  membranes 
alone  protrude  into  the  sac. 

2.  Spinal  meningo-myelocele  is  a  form  in  which  the  membranes  and 
cord  both  protrude. 

3.  Syringo-myelocele  (hydrorrhachis  interna)  is  a  form  in  which  the 
fluid  is  in  the  central  spinal  canal,  and  the  inner  lining  of  the  sac  is 
formed  by  the  meninges  and  thinned-out  spinal  cord. 

Anatomy. — -The  first  two  forms  are  the  most  common  and  are  called 
hydrorrhachis  externa.  The  fluid  here  lies  in  the  subarachnoid  sac, 
and  hence  the  wall  of  the  protruding  cyst  is  lined  with  the  dura  and 
arachnoid.  The  nerves  and  cord  protrude  into  the  sac  in  two-thirds  of 
the  cases  (forming  a  meningo-myelocele),  but  in  some  of  these  only  a  few 
nerves  are  found.     These  structures,  when  present  in  the  sac,  as  in  men- 


a  hca 


a  bca 


a  bca 


Fig.  96. 


u      a  u     a  u     a, 

-Meningocele.    Meningo-myelocele.     Syringo-myelocele. 
walls;  6,  cord;  c,  membranes. 


a,  Vertebral 


ingo-myelocele,  lie  on  its  posterior  and  median  surface.  They  are  attached 
to  and  form  part  of  the  wall.  The  spinal  nerves  therefore  start  from 
the  wall  of  the  sac  and  go  back  into  the  vertebral  canal.  The  tumor  con- 
tains cerebrospinal  fluid,  and  occasionally  connective  tissue  and  fat  (Fig. 
97).  The  external  surface  is  often  red  and  smooth,  and  there  is  some- 
times a  depression  on  its  median  surface  where  the  cord  is  attached. 

Symptoms. — Spinal  bifida  occurs  almost  always  in  the  lumbar  and 
sacral  region,  the  reason  being  that  the  laminae  here  are  the  last  to  solid- 
ify.    Usually  but  two  or  three  vertebrae  are  involved. 

The  tumor  varies  in  size  from  3  cm.  (1  in.)  to  15  cm.  (6  in.)  in  diam- 
eter, and  may  have  a  broad  base  or  be  pedunculated.  The  outer  skin 
is  often  glossy,  or  tough,  thickened  or  ulcerated. 

Children  with  spina  bifida  are  usually  feeble,  badly  nourished  and 
poorly  developed  mentally.  Paraplegia  occurs  in  half  the  cases,  sometimes 
with  anaesthesia  and  involvement  of  the  sphincters.  Talipes  occurs  quite 
often. 


216  DISEASES    OF    THE    NEEVOUS    SYSTEM 

The  prognosis  is  grave.  Most  subjects  die  unless  treatment  is  applied, 
and  even  then  the  prospect  is  not  very  good.  The  prognosis  is  best  for 
meningocele. 

The  diagnosis  is  easy.  It  is  generally  only  necessary  to  exclude  con- 
genital tumors  which  happen  to  be  located  in  the  lumbo-sacral  region. 
The  most  important  question  to  decide  is  whether  the  cord  and  nerves  are 
present  in  the  sac.  This  may  be  assumed  as  probable  if  there  is  much 
paraplegia,  anaesthesia  and  sphincter  trouble,  and  if  there  is  a  depression 
on  the  median  external  surface.  The  introduction  of  an  insulated  needle 
connected  with  an  electric  battery  may  be  tried. 

The  treat?nent  is  strictly  surgical,  and  then  is  of  avail  only  in  meningo- 
cele.    Injections   of   Morton's   fluid    (iodine,   gr.   x.;   potas.   iodid.,   gr. 


Fig.  97. — Spina  bifida. 

XXX.;  glycerin,  §i.  Dose,  §i)  have  been  successful.  These  injections 
should  be  made  in  the  lateral  portion  of  the  sac,  and  the  child  should  be 
kept  on  the  back.  Puncture  and  withdrawal  of  fluid  with  compression 
is  not  a  justifiable  operation.  Ligaturing  or  opening  and  excising  of  the 
sac  are  dangerous,  especially  if,  as  is  often  the  case,  part  of  the  cord  and 
nerves  lie  in  the  sac.  In  recent  years,  surgical  results  have  been  more 
favorable  and  warrant  serious  consideration.  No  surgical  treatment 
should  be  attempted,  however,  until  two  or  three  months  after  birth, 

OTHER  MALFORMATIONS 

Heteropia  is  a  rare  malformation  in  which  masses  of  gray  matter  are 
found  in  abnormal  situations.  A  false  heteropia  may  be  caused  by 
manipulation  of  the  cord  in  its  removal  after  death.  The  displaced 
masses  consist  of  nerve-cells  or  neuroglia. 

Amyelia,  or  absence  of  the  spinal  cord,  can  exist  only  when  the 
brain  is  absent;  but  absence  of  the  brain  may  occur  without  absence  of  the 


DISEASES    OF    THE    SPINAL    CORD  217 

cord.  In  amyelia  the  spinal  nerves  are  usually  present.  Amyelic 
monsters  cannot  live. 

Double  cord  is  a  very  rare  defect  and  involves  only  part  of  the  cord 
except  in  cases  in  which  there  is  a  double  vertebral  canal.  It  occurs 
sometimes  in  connection  with  spina  bifida. 

Double  central  canal  is  not  rare.  It  usually  involves  only  a  part  of  the 
cord.     The  two  canals  are  side  by  side. 

Asymmetry  of  the  cord,  usually  due  to  abnormality  in  the  course 
of   the    pyramidal   tracts,    is    not    extremely   rare. 

Splitting  of  the  cord  and  defects  in  development  at  special  levels  are 
occasionally  observed. 

Micromyelia  is  a  condition  in  which  the  spinal  cord  is  abnormally  short 
or  small  in  size,  and  is  not  a  very  rare  anomaly.  The  normal  adult  cord 
has  a  diameter  in  its  various  parts  of  6  to  9  mm.  (dorsal),  8  to  11  mm. 
(upper  cervical),  15  mm.  (cervical  swelling),  and  12  mm.  (lumbar). 

SPINAL  HEMORRHAGE   (SPINAL  APOPLEXY) 

This  general  name  may  be  given  to  (1)  spinal  meningeal  hemorrhage 
or  hsematorrhachis,  and  (2)  hemorrhage  into  the  cord  substance,  or 
haematomyelia. 

1.  Spinal  meningeal  hemorrhage  is  far  the  most  common  form.  It 
may  be  outside  or  inside  of  the  dura,  the  former  being  rather  oftener  seen. 

Etiology. — It  occurs  in  newly  born  children  and  in  adults,  and  is 
more  common  in  men  than  in  women.  Injuries,  falls,  fractures  of  the 
spine  are  the  most  frequent  exciting  causes.  Severe  convulsions  from 
epilepsy,  eclampsia,  tetanus,  chorea  or  strychnine  and  even  severe 
muscular  exertion  may  be  a  cause.  Childbirth,  purpura  and  the  blood 
states  following  malignant  infectious  fevers,  bursting  of  an  aortic  or 
vertebral  aneurism,  and  cerebrospinal  meningitis  are  rare  causes. 

Symptoms. — In  small  hemorrhages  there  may  be  no  symptoms. 
In  large  effusions  there  are  sudden  very  severe  pains  in  the  back,  extend- 
ing into  the  limbs  with  numbness,  tingling,  hyperesthesia  and  mus- 
cular spasm,  especially  of  the  back  muscles.  Later  there  may  be  weak- 
ness or  paralysis  and  anaesthesia  of  the  extremities,  with  disorder  of 
the  visceral  centres.  The  reflexes  are  exaggerated.  The  distribution  of 
the  anaesthesia  may  be  segmental  unless  the  hemorrhage  is  very  large. 
The  symptoms  reach  their  height  usually  in  a  few  hours.  Then  ameliora- 
tion may  occur,  followed  by  slow  recoveiy  or  with  symptoms  of  chronic 
meningitis.     Rarely  death  occurs  early  from  exhaustion. 

Diagnosis. — A  history  of  injury  or  childbirth,  sudden  onset  of  attack, 
with  symptoms  of  pain  and  meningeal  irritation  with  rigidity  which 
rather  rapidly  subside,  point  to  extra-dural  hemorrhage.  In  haemato- 
myelia there  are  less  pain  and  irritation,  but  more  profound  paralysis  and 


218  DISEASES    OF    THE    NERVOUS    SYSTEM 

anaesthesia.  The  same  is  true  of  crush  of  the  cord  from  fracture  or  dislo- 
cation. In  tetanus  there  is  a  slower  development  of  the  symptoms  and 
trismus  is  present.     Lumbar  puncture  will  assist  the  diagnosis. 

The  prognosis  is  grave  in  severe  cases,  but  if  the  patient  survives  three 
or  four  days  the  prospect  of  partial  or  nearly  complete  recovery  is  good. 
The  treatment  is  perfect  rest  in  bed  and  the  administration  of  remedies 
to  move  the  bowels  and  relieve  pain;  leeches  and  other  local  applications 
are  of  doubtful  value.  If  there  is  distinct  evidence  of  fracture  or  disloca- 
tion surgical  interference  may  be  indicated.  It  is  of  no  use  to  give  styptics 
except  in  purpura,  when  mineral  acids  or  suprarenal  extract  may  be  tried. 
Later,  one  may  give  iodide  and  mercury  and  use  blisters  to  the  back. 

2.  Hemorrhage  into  the  Substance  of  the  Cord  (Haematomyelia)^ 
Etiology. — The  condition  is  not  very  rare.  It  may  be  primary  from  dis- 
ease of  the  blood-vessels  or  purpura  hemorrhagica;  or  it  may  be  secondary 
to  myelitis  and  tumors.  Primary  hemorrhage  occurs  sometimes  in  in- 
fancy, but  usually  in  males  between  the  twentieth  and  fortieth  years. 
Infection,  injuries,  over-exertion  and  exposure,  excessive  coitus  (Gowers), 
syphilitic  disease  of  the  blood-vessel,  and  convulsions  are  causes.  The  dis- 
ease sometimes  occurs  in  old  people  with  degenerated  arteries,  which  break 
and  lead  to  a  spinal  apoplexy,  just  as  occurs  in  the  brain.  More  often  the 
condition  in  old  people  is  a  thrombosis.  A  special  cause  of  spinal  hemor- 
rhage is  working  under  high  atmospheric  pressure,  as  in  the  caisson  disease. 

The  symptoms  develop  rapidly,  with  at  first  feelings  of  numbness  or 
weakness  for  one  or  two  hours  or  longer.  Then  there  is  a  sudden  para- 
plegia, with  anaesthesia  or  ataxia  or  both.  The  anaesthesia  is  often  dis- 
sociated, there  being  loss  of  pain  and  thermic  sense  with  retention  of 
considerable  tactile  sense.  The  sphincters  may  be  paralyzed;  the  urine 
has  to  be  drawn.  The  reflexes  may  be  abolished  at  first,  but  soon  return 
and  become  exaggerated  with  signs  of  pyramidal  tract  involvement. 
There  is  considerable  pain  in  the  back.  If  the  lesion  is  high  up,  the 
arms  and  thorax  are  involved.  The  acute  symptoms  begin  usually  to 
subside  at  the  end  of  seven  to  ten  days  and  the  disease  takes  the  char- 
acter of  a  chronic  myelitis.  If  improvement  does  not  occur,  evidences 
of  acute  myelitis  or  softening  appear  and  the  patient  dies. 

Pathology. — The  vessels  involved  are  the  central  arteries,  which  sup- 
ply the  gray  matter  and  are  under  relatively  high  pressure.  The  rupture 
of  the  vessel,  when  due  to  disease,  is  caused  by  a  fatty  degeneration  of 
the  coats  or  endarteritis;  miliary  aneurisms,  such  as  are  found  in  the 
brain,  rarely  develop  in  the  cord.  Hemorrhage  often  precedes  or  be- 
gins a  myelitis,  of  which  it  may  be  the  cause  or  the  result.  The  clot 
may  be  absorbed,  leaving  a  cavity  as  in  the  brain;  or  the  broken-down 
tissue  may  become  the  centre  of  a  myelitic  focus.  The  hemorrhage  is 
usually  single,  but  there  may  be  several.     Multiple  capillary  hemorrhages 


DISEASES    OF    THE    SPINAL    CORD  219 

occur,  but  usually  only  from  asphyxia  and  convulsions  or  in  caisson  dis- 
ease. It  is  possible  that  some  of  the  cases  of  disseminated  myelitis  oc- 
curring after  infectious  fevers  start  from  small  hemorrhages.  Hemor- 
rhage sometimes  results  from  the  invasion  of  the  cord  by  a  new  growth,  as 
in  syringomyelia. 

Diagnosis. — The  points  to  be  noted  are  the  sudden  onset  without 
long  premonitory  symptoms,  and  the  absence  of  fever  followed  later  by 
gradual  improvement.  There  is  much  less  pain  and  more  paralysis  than 
in  meningeal  hemorrhage,  and  the  dissociation  of  cutaneous  sensations 
is  very  characteristic.  In  acute  softening  there  is  less  of  the  dissociation 
of  sensations  and  usually  a  more  extensive  paralysis  and  the  patient  is 
syphilitic  or  aged.  The  disease  is  often  mistaken  for  acute  primary 
myelitis,  which  does  in  fact  sometimes  follow  it. 

Prognosis. — This  is  often  serious  as  regards  life,  and  always  serious 
as  regards  health.  It  depends  on  the  extent  and  seat  of  the  hemorrhages. 
Dorsal  hemorrhages  are  more  favorable,  cervical  the  least. 

Treatment. — Absolute  rest,  ice  bags  to  the  spine,  and  small  doses  of 
aconite  given  early  are  all  that  can  be  tried,  except  the  use  of  sympto- 
matic remedies.  Treatment  must  be  applied  at  once.  The  late  treat- 
ment is  the  same  as  that  for  chronic  myelitis. 

THE  CAISSON  DISEASE   (DIVER'S  PARALYSIS) 

The  caisson  disease  is  the  name  given  to  a  group  of  symptoms  char- 
acterized mainly  by  pains  and  paralysis  which  occur  in  persons  who 
work  in  caissons  or  diving  bells,  and  which  are  brought  about  by  the 
sudden  return  from  condensed  air  to  the  normal  atmosphere. 

Etiology. — Persons  employed  in  caissons  or  bells  work  usually  under 
a  pressure  of  from  one  to  four  atmospheres,  which  means  a  pressure  of 
from  fifteen  to  fifty  pounds  to  the  square  inch.  Accidents,  rarely,  if  ever, 
occur  if  the  pressure  is  not  over  one  atmosphere,  and  they  are  rare  if  the 
person  has  not  been  subjected  to  the  pressure  for  at  least  an  hour.  The 
effective  cause  of  the  symptoms,  however,  is  a  too  rapid  decompression. 
Different  persons  vary  in  susceptibility  to  the  effects  of  this  change  in 
the  atmospheric  pressure,  and  those  unused  to  the  work  or  of  maturer 
age  and  poor  arteries  are  more  liable  to  be  attacked.  Naturally,  the 
disease  is  seen  only  in  men,  and  during  the  working  period  of  life.  Hunger 
and  exhaustion  make  a  person  more  susceptible. 

The  symptoms  set  in  usually  very  soon  after  the  patient  has  come  out 
from  the  caisson,  but  they  may  be  delayed  for  half  an  hour  to  an  hour. 
They  consist  of  intense  neuralgic  pains  in  the  lower  extremities,  often 
affecting  especially  the  joints.  There  is  at  the  same  time  epigastric  pain. 
Nausea  and  vomiting  with  weakness  in  the  lower  limbs,  amounting  in 
some  cases  to  absolute  paralysis,  very  soon  appear.     There  may  be 


220 


DISEASES    OF    THE    NERVOUS    SYSTEM 


headache,  dizziness,  and  sometimes  choking,  coughing  and  oppression 
in  breathing.  If  the  paralysis  is  considerable,  it  is  usually  accompanied 
by  anaesthesia.  Disturbances  in  the  sphincters,  with  retention  of  urine 
and  constipation,  may  also  be  present.  The  symptoms  vary  very  much 
in  severity,  from  pain,  weakness  in  the  legs  and  nausea,  up  to  frightful 
neuralgic  attacks  and  complete  paralysis,  motor  and  sensory.  The 
upper  limbs  are  rarely  affected.  The  disease  lasts  from  a  few  hours  up 
to  several  weeks.  Death  occurs  in  some  of  the  very  severe  cases.  The 
symptoms  having  reached  their  climax  gradually  ameliorate,  and  a  com- 
plete cure  is  not  infrequent.  In  some  instances,  however,  the  patient 
is  left  with  a  permanent  paraplegia  and  the  ordinary  symptoms  of  a 


Fig.  98. — Spinal  cord  in  caisson  disease  showing  extensive  destruction  of  tissue. 

transverse  myelitis.  Hemiplegia  occurs  in  about  one-fifth  of  cases  and 
still  more  rarely  a  monoplegia. 

The  disease  in  its  mildest  form  is  characterized  mainly  by  severe  pains, 
with  some  weakness  and  dizziness  which  usually  soon  pass  away.  The 
symptoms  are  spoken  of  as  "the  bends."  When  vertigo  and  staggering 
and  some  mental  confusion  are  dominant,  it  is  called  ''the  staggers," 
and  the  dyspnceic  and  coughing  attacks  are  called  "the  chokes." 

Pathology. — When  the  patient  is  under  atmospheric  pressure  in-the 
caisson,  the  blood  is  driven  from  the  surface  of  the  body,  and  the  internal 
viscera,  including  the  brain  and  cord,  are  congested.  The  sudden  change 
from  the  abnormal  to  normal  pressure  produces  a  rapid  flow  of  blood  from 


DISEASES    OF   THE    SPINAL    COED  221 

the  internal  organs  to  the  periphery.  The  viscera  not  inclosed  in  bony 
cavities  are  enabled  to  relieve  themselves  of  this  congestion  without 
much  harm,  but  the  circulation  in  the  brain  and  spinal  cord  is  less  elastic; 
that  in  the  spinal  cord  being  less  even  than  that  in  the  brain.  The  result 
is  that  congestions  and  small  hemorrhages  ensue,  producing  a  destruction 
•of  the  nerve-tissue.  In  other  cases  there  seems  to  be  a  blocking  up  of 
some  of  the  small  vessels,  with  consequent  softening  of  different  portions 
of  the  cord  and  to  a  less  extent  of  the  brain.  The  most  important  ele- 
ment in  causing  the  trouble  is  the  escape  of  oxygen  and  carbonic-acid  gas 
from  the  blood  into  the  tissues  or  into  the  blood-vessels,  forming  gas 
emboli.  It  will  be  seen,  however,  that  on  the  whole  the  serious  organic 
changes  consist  in  the  vascular  disturbances  with  rupture  or  obliteration 
of  blood-vessels,  and  consequent  destruction  and  necrosis  of  tissue. 
Following  this  is  a  reactive  inflammation  producing  the  phenomena  of 
a  reactive  acute  myelitis. 

Prognosis. — The  painful  and  vertiginous  types  of  the  trouble  nearly  all 
get  well.     Over  half  of  the  paralytic  cases  recover. 

Prophylaxis. — The  safest  age  for  caisson  workers  is  from  twenty  to 
thirty-five.  They  should  have  a  good  muscular  system,  good  eyes,  ears, 
lungs  and  hearts.  The  Anglo-Saxons  and  negroes  seem  to  stand  the  work 
better  than  the  Latin  races  (Pelton).  They  should  not  have  the  status 
lymphaticus.  They  should  drink  but  little.  The  most  important  pre- 
caution of  all  is  slow  decompression,  about  two  pounds  per  minute.  Hill 
and  Greenwood  assert  that  pressures  up  to  seven  atmospheres  (about 
140  pounds  to  the  square  inch)  can  be  safely  borne,  if  the  decompres- 
sion is  slow  enough.  On  coming  out  the  workmen  should  not  do  any 
climbing,  and  should  not  take  hot  coffee,  nor  alcohol,  as  a  drink. 

Treatment. — The  most  essential  thing  for  immediate  treatment  and 
relief  is  immediate  recompression  in  a  hospital-lock  provided  for  the  pur- 
pose. The  pressure  (Pelton)  should  be  gradually  increased  to  about  that 
under  which  the  patient  has  worked.  Then  in  a  few  minutes  decompres- 
sion is  very  slowly  given. 

When  the  disease  has  developed  it  can  be  treated  only  by  symptomatic 
remedies.  The  patient  should  be  kept  quiet,  and  given,  if  necessary, 
hypodermatics  of  morphine.  Dr.  A.  H.  Smith  recommends  the  use  of 
ergot.  Later  on,  the  various  neuralgic  and  paralytic  symptoms  may  be 
treated  on  the  same  principles  as  those  employed  in  myelitis. 

INFLAMMATION   OF   THE    SPINAL   MEMBRANES    (SPINAL   MENINGITIS) 

The  meningeal  inflammations  acute  and  chronic  are: 

Pachymeningitis.  |  Affecting  the  dura  mater. 

Leptomeningitis.  J  Affecting  the  pia  mater. 

,,     .  ,.^.  I  Affecting  both  membranes 

Menmgo-myelitis.  ■  i  i         i 


222  DISEASES    OF   THE    NEEVOUS   SYSTEM 

EXTERNAL  MENINGITIS,  PACHYMENINGITIS  EXTERNA 

Etiology. — The  disease  is  rare,  and  always  occurs  secondarily  to  some 
other  morbid  process.  This  process  is  in  most  cases  tuberculosis  causing 
caries  of  the  vertebrae.  Other  causes  are  suppurative  inflammation,  such 
as  a  carbuncle,  in  the  neighborhood  of  the  vertebrae,  psoas  abscess,  puru- 
lent pleurisy,  and  the  extension  of  a  neoplasm.  Tuberculous  pachy- 
meningitis is  so  commonly  associated  with  cord  changes  that  it  is  de- 
scribed more  fully  under  the  head  of  Compression  Myelitis. 

Symptoms. — The  symptoms  are  those  of  irritation  of  the  motor  and 
sensory  roots;  later  of  compression  of  them  and  of  the  spinal  cord.  There 
occur  local  pains  in  the  back,  radiating  pains,  local  tenderness,  and  hyper- 
sesthesia,  twitching  of  muscles  and  rigidity  of  spine,  progressive  develop- 
ment of  a  fLpastic  paraplegia,  exaggeration  of  reflexes,  and  involvement 
of  the  sphincters.  Anaesthesia  occurs  in  severe  forms,  which  takes  the 
distribution  of  a  root  anaesthesia. 

The  disease,  when  chronic,  may  extend  to  the  other  membranes  and 
cord,  causing  chronic  meningo-myelitis. 

Pathological  Anatomy. — The  inflammation,  if  acute,  is  generally  a 
fibro-purulent  one.  The  dura  mater  is  covered  by  a  layer  of  caseous, 
semisolid  matter,  often  very  thick  and  most  extensive  posteriorly.  It 
involves  the  dura  vertically  for  several  inches.  In  chronic  forms  the 
deposit  is  made  up  of  connective  tissue  and  the  cord  is  compressed.  In 
purely  suppurative  forms  the  cellular  tissue  outside  the  dura  is  infiltrated 
with  pus  throughout  a  great  part  of  the  canal. 

The  diagnosis  is  based  on  the  presence  of  the  primary  local  disease,  a 
kyphosis,  the  radiating  pains,  and  tenderness  and  by  the  combination  of 
motor  and  sensory  irritation  and  paralysis.  Anaesthesia  and  sphincter 
troubles  come  late  in  the  disease. 

The  prognosis  is  bad,  if  the  original  disease  is  a  serious  one.  Still, 
surprisingly  good  results  are  often  obtained  when  the  disease  is  taken 
early,  especially  in  tuberculosis  cases. 

The  treatment  consists  in  attention  to  the  local  caries  or  inflammatory 
focus.     It  is  therefore  purely  surgical,  mechanical  and  symptomatic. 

PACHYMENINGITIS  INTERNA 

{Hypertrophic  Cervical  Pachymeningitis) 

Inflammation  of  the  inner  surface  of  the  dura  mater  has  been  much 
written  about,  and  but  little  seen.  It  is  almost  always  only  a  syphilitic 
meningo-myelitis  and  it  attacks  the  cervical  region  as  a  rule. 

Etiology: — The  disease  occurs  always  in  adult  life.  It  usually 
affects  males.     Syphilis  and  trauma  are  the  causes. 


DISEASES    OF    THE    SPINAL    CORD  223 

Symptoms. — The  disease  begins  gradually  with  symptoms  of  irrita- 
tion (irritative  stage) .  The  patient  suffers  from  pain  and  stiffness  in  the 
neck.  The  pains  radiate  up  to  the  occiput  and  down  the  back;  numb- 
ness, prickling  and  pain  are  felt  in  the  arms,  more  in  one  than  the  other. 
The  pains  exacerbate  and  are  worse  at  night.  Stiffness  and  cramps  may 
affect  the  arms.     Nausea  and  vomiting  sometimes  occur. 

After  five  or  six  months,  symptoms  of  paralysis  appear  (paralytic 
stage).  The  arms  are  affected.  They  become  weak,  atrophy  occurs, 
associated  with  contractures  and  rigidity.  There  is  still  pain,  and  in 
addition  anaesthesia,  hypersesthesia  and  trophic  changes  occur.  Later, 
paraplegia,  with  rigidity,  exaggerated  reflexes,  and  spinal  trepidation 
develop.  The  patient  becomes  weaker,  and  finally  dies  of  exhaustion  or 
from  some  intercurrent  trouble.  Usually  it  runs  along  and  painful  course, 
but  if  early  recognized  and  treated  it  should  be  at  least  controlled. 

Pathology. — The  disease  starts  as  an  inflammatory  syphilitic  exudate 
upon  the  surface  of  the  dura.  This  leads  to  a  chronic  inflammatory 
process,  and  finally  the  cord  is  encircled  and  compressed  by  a  dense 
laminated  connective-tissue  mass,  which  involves  the  pia  and  to  some 
extent  the  cord  substance. 

Diagnosis. — This  must  be  made  from  tumor,  myelitis,  Pott's  disease, 
wry-neck  and  progressive  muscular  atrophy.  The  history  of  injury,  the 
slow  progressive  course,  and  the  localization  of  the  symptoms,  their 
bilateral  character  and  the  pain,  a  history  and  laboratory  evidence  by 
lumbar  puncture  of  syphilitic  infection  give  adequate  help.  In  spinal 
tumor  the  symptoms  at  the  beginning  are  more  sharply  localized.  They 
develop  more  rapidly  and  the  course  of  the  disease  is  shorter  than  in 
meningitis. 

Treatment. — The  syphilitic  origin  of  the  disease  must  be  borne  in 
mind.  Counterirritants,  electricity,  hydrotherapy  and  symptomatic 
remedies  for  the  pain  and  spasms  are  indicated. 

ACUTE  SPINAL  LEPTOMENINGITIS 

(Inflammation  of  the  Pia  Mater  of  the  Spinal  Cord) 

Etiology. — This  is  so  rare  a  disease,  occurring  alone,  that  I  leave  it  out 
of  the  category  of  independent  disorders.  The  description  of  cerebro- 
spinal meningitis  covers  sufficiently  the  ground. 

CHRONIC  LEPTOMENINGITIS  (NON-LUETIC) 

Etiology. — This  disease,  which  used  to  be  often  diagnosticated,  is  now 
believed  to  be  rare  and  always  secondary  to  trauma,  or  an  acute  process, 
such  as  a  cerebrospinal  meningitis.     It  occurs  oftenest  in  adults  and  in 


224  DISEASES    OF    THE    NEEVOUS    SYSTEM 

males.  Trauma,  and  especially  concussion  of  the  spine,  used  to  be 
thought  a  frequent  cause,  but  in  most  of  such  cases  the  trouble  is  simply 
a  hypersemia  or  else  is  neuralgic  and  functional. 

The  sympto7ns  gradually  develop  after  an  acute  meningitis  or  an  injury, 
they  are. similar  in  character  to  those  of  the  acute  process.  There  are 
pain  in  the  back,  increased  on  movement  and  radiating  about  the  trunk  and 
down  the  limbs,  tenderness  along  the  spine,  stiffness  of  the  back,  twitching 
and  spasms  in  the  limbs  with  some  weakness.  The  symptoms  run  an 
irregular  course  with  periods  of  improvement. 

Pathological  Anatomy. — The  inflammation  consists  of  a  proliferation 
of  connective  tissue  (productive  inflammation  of  Delafield) .  The  result 
is  a  thickening  and  opacity  of  the  pia  mater  and  arachnoid. 

The  diagnosis  must  be  made  from  functional  disease,  meningo- 
vascular syphilis,  myelitis,  and  vertebral  caries. 

In  vertebral  caries  the  pain  and  tenderness  are  much  more  localized, 
and  there  is  spasmodic  fixation  of  the  trunk.  The  pain  is  more  continuous 
and  dull,  and  is  increased  by  lateral  pressure  and  lessened  by  extension. 
There  is  usually  also  some  deformity.  If  compression  occurs  there  is 
exaggeration  of  the  reflexes  and  paraplegia  without  much  anaesthesia. 

Treatment. — Chronic  meningitis  not  the  product  of  syphilis  is  the  relic 
of  traumatism  or  of  an  acute  process  and  the  indications  for  treatment  are 
simple.  Rest  is  the  essential  thing.  With  this  can  be  combined  the  sys- 
tematic and  persistent  use  of  counterirritants.  The  hot  iron  is  usually 
best,  because  its  wounds  heal  so  quickly.  Cupping  is  also  useful  if  done 
vigorously  and  often. 

MYELITIS   AND    MYELOMALACIA— INFLAMMATION  AND  SOFTENING  OF 

THE  SPINAL  CORD 

Inflammation  of  the  spinal  cord  is  known  as  myelitis.  Softening  of  the 
cord  is  known  as  myelomalacia.  The  processes  are  practically  associated. 
Acute  myelitis  always  ends  in  some  form  of  softening ;  and  acute  softening 
is  often  followed  by  reactive  or  infective  inflammation.  If  inflammation 
affects  the  gray  matter  only  it  is  called  poliomyelitis ;  and  if  the  anterior 
horns  chiefly,  it  is  an  anterior  poliomyelitis.  Both  the  gray  and  white 
matter  are  usually  affected,  and  myelitis  or  spinal  softening  may  be  dif- 
fuse, disseminated,  or  transverse  in  accordance  with  the  distribution  of 
the  process.  The  forms  are  still  further  divided,  in  accordance  with  their 
location,  into  the  cervical,  dorsal,  and  lumbar.  Myelitis  is  given  different 
names  also  in  accordance  with  its  cause.  Thus  we  have  hemorrhagic 
myelitis,  a  form  in  which  the  process  is  due  to  or  associated  with  a 
hemorrhage;  compression  myelitis,  due  to  vertebral  caries  and  the  pressure 
of  tuberculous  exudate,  purulent  myelitis  or  abscess  of  the  cord;  and 


DISEASES    OF    THE    SPINAL    CORD 


225 


tuberculous  and  syphilitic  myelitis  which  are  really  essentially  necrotic 
and  softening  processes  and  not  myelitic. 

The  following  table  will  show  the  different  morbid  processes  and  the 
six  clinical  types  of  myelitis: 


Forms  of  Myelitis  and  Myelomalacia 


Pathological  Process 


Clinical  Type 


An   exudative,   lymphogenous   inflamma-1. 
tion  due  to  infection. 


Anterior  poliomyelitis,  Landr3^'s  acute 
ascending  paralysis. 


An  exudative,  hemorrhagic  or  purulent  in-  2. 
flammation  due  to  infection. 


Acute  transverse,  diffuse  and  dissemin- 
ated myelitis. 
Abscess  of  cord  (rare). 


A    subacute    degenerative     and    necrotic  4. 
process  due  to  toxins. 


Subacute    combined   and    diffuse    cord 
degenerations  (combined  sclerosis). 


An  embolic  or  thrombotic  process. 


5.  Acute  and  subacute  softening  of  cord. 


A  parenchymatous  degeneration  with  con- 6. 
nective-tissue  proliferation  due  to  vas- 
cular and  toxic  causes,  or  secondary 
processes. 


Subacute    and    chronic    poliomj^elitis. 


Acute  myelitis  is  a  local  or  diffuse  exudative  inflammation  with  more 
or  less  necrosis  and  softening.     (Type  2  of  table.) 

Etiology. — It  affects  adults  in  early  and  middle  life,  and  men  oftener 
than  women.  It  is  rarely  seen  in  old  age  or  childhood.  Heredity  and 
neuropathic  constitution  are  not  important  factors,  though  it  is  probable 
that  there  are  some  persons  whose  spinal  cords  are  less  resistant  to  infec- 
tion than  others. 

Exposure  to  cold,  bodily  and  sexual  excesses,  and  violent  concussion 
have  some  importance  indirectly  in  favoring  the  entrance  of  infection. 

The  list  of  local  bodily  infections  which  are  the  source  from  which  the 
cord  becomes  infected  is  very  long  and  includes  general  sepsis,  peritonitis, 
appendicitis,  enteritis,  colitis,  liver  abscess,  cystitis  (urinary  paraplegia) , 
gonorrhoea,  osteomyelitis,  and  tonsillitis.  It  more  rarely  follows  general 
infections,  such  as  influenza,  small-pox,  scarlet  fever,  typhoid  fever, 
rheumatism,  diphtheria,  and  pneumonia.  Sometimes  the  micro-organ- 
ism of  acute  poliomyelitis  causes  a  definite  transverse  or  diffuse  myelitis. 
Myelitis  has  occurred  associated  with  the  toxaemia  of  pregnancy.  In 
this  and  perhaps  other  infections  or  toxsemias  the  lesion  may  be  due  to 
thromboses  from  the  increased  coagulability  of  the  blood  or  circulatory 

15 


226  DISEASES    OF    THE    NERVOUS    SYSTEM 

weakness.  The  infection  of  polyneuritis  in  rare  cases  may  affect  the 
cord  also. 

Certain  chemical  poisons  such  as  carbonic  oxide,  sulphide  of  carbon, 
and  chloroform  cause  a  necrotic  and  degenerative  rather  than  an  exuda- 
tive myelitis. 

Syphilis  does  not  cause  acute  myelitis  but  only  softening  with  hemor- 
rhages and  chronic  degenerative  changes. 

The  mechanical  injury  due  to  gas  bubbles  in  caisson  disease  may 
destroy  cord  tissue  and  lead  to  inflammatory  changes. 

Despite  the  above  long  list,  acute  myelitis  is  really  a  very  rare  disease. 

Symptoms. — The  initial  symptoms  consist  of  feelings  of  numbness, 
usually  in  the  feet  and  legs,  which  seem  heavy  and  weak.  Some  pain 
may  be  felt  about  the  back.  The  patient  finds  that  he  cannot  walk 
easily,  that  he  moves  his  legs  with  an  effort  and  that  they  feel  stiff.  In 
one  or  two  days  some  paraplegia  with  ansesthesia  has  developed,  and  if 
the  lesion  is  in  the  cervical  cord  the  arms  are  paralyzed  also.  Partial 
or  complete  retention  or  incontinence  of  urine  and  constipation  occur  at 
the  same  time.     There  may  be  some  fever. 

In  three  or  four  days,  sometimes  in  a  day,  the  disease  reaches  nearly 
its  height  and  the  patient  is  paraplegic  and  confined  to  bed. 

If  the  patient  is  now  examined  it  will  be  found  that  he  cannot  walk 
or  stand,  but  can  move  his  legs  a  little.  He  complains  of  a  sensation 
like  a  band  around  his  waist  or  at  the  level  of  the  spinal  lesion  (girdle 
symptom).  His  legs  feel  numb  and  heavy,  but  there  is  little  pain  and 
no  tenderness.  Ansesthesia  to  touch,  pain,  and  temperature  and  of  deep 
sensibility  exists,  in  varying  degree  according  to  the  seriousness  of  the 
case,  as  high  up  as  the  lesion.  The  anaesthesia,  if  not  total,  is  greatest  to 
touch,  next  to  temperature  and  to  pain  and  least  to  sense  of  position  and 
deep  pain.  The  bladder  is  anaesthetic;  the  urine  is  retained,  and  has  to 
be  drawn.  The  bowels  are  constipated,  and  if  enemata  are  given  the 
faeces  may  pass  away  without  his  knowledge,  owing  to  rectal  ansesthesia. 
If  the  lesion  is  lumbar,  there  is  abolition  of  the  sexual  power;  but  if  dorsal 
or  cervical,  erections  may  occur  without  the  patient's  feeling  them. 
When  the  lesion  is  above  the  lumbar  cord  also,  the  bladder  may  auto- 
matically and  forcibly  contract  and  expel  the  urine.  In  time  the  bowels 
regain  some  power.  The  paralysis  in  the  limbs  affects  the  extensors 
more  than  the  flexors  of  the  toes,  the  flexors  of  the  feet  and  legs  more  than 
the  extensors.  The  patient  can  push  down  his  limbs  better  than  he  can 
draw  them  up  and  he  can  adduct  better  than  abduct. 

The  temperature  of  the  limbs  for  a  few  days  may  be  raised,  but  after 
this  it  may  fall  a  few  degrees  below  normal.  The  skin  becomes  rough, 
cold,  congested;  or  excessive  perspiration  may  take  place.  The  general 
bodily  temperature  is  usually  normal  throughout  the  disease,  but  in 


DISEASES    OF    THE    SPINAL    CORD 


227 


some  cases  septic  fever  develops  of  102°  to  104°  and  continues.  The  pi'og- 
nosis  is  then  bad. 

Bed-sores  may  develop  early,  within  a  few  days  or  weeks  unless  great 
care  be  taken.  They  appear  oftenest  upon  the  buttocks  and  heels,  and 
are  due  to  vascular  weakness  trophic  disturbance,  combined  with  pres- 
sure and  pyogenic  infection  of  the  parts.  Bed-sores  are,  however,  not 
necessary  if  every  possible  care  and  precaution  are  taken. 

If  the  lesion  is  lumbar,  the  tendon  and  skin  reflexes  are  lessened 
and  the  paralysis  is  somewhat  flaccid.  The  muscles  also  tend  to  waste 
and  show  degenerative  reactions.  If  the  lesion  is  dorsal,  as  is  more  often 
the  case,  the  reflexes  are  present,  and  after  a  time  become  exaggerated; 


Fig.  99. — Acute  transverse  myelitis  of  lumbar  cord,  showing  distribution  of 
anaesthesia.'  Area  in  lines  =  total  anaesthesia  and  analgesia.  Dotted  area  =  anal- 
gesia only. 


there  is  ankle  clonus  and  extensor  response  on  irritating  the  soles  of  the 
feet;  contractures  and  spasms  develop;  the  legs  become  drawn  up  and 
deformities  are  produced.  If  the  lesion  is  so  complete  as  entirely  to  cut 
across  the  cord,  there  may  still  be  some  excessive  muscular  tension,  but 
the  reflexes  will  be  abolished.  When  the  cervical  region  is  attacked, 
the  arms  are  involved  as  well  as  the  legs,  with  a  segmental  lower  motor 
neuron  palsy,  generally  severer  in  the  arms.  There  may  now  be  also 
unequal  dilatation  of  the  pupils  from  involvement  of  the  cilio-spinal 
centre.  In  extensive  involvement  of  the  upper  part  of  the  cord  there 
will  be  paralysis  of  the  intercostal  muscles  and  disturbance  of  the  heart's 
action. 


228 


DISEASES    OF    THE    NERVOUS    SYSTEM 


The  disease,  having  in  a  few  days  reached  its  height,  usually  remains 
stationary  for  a  few  weeks,  and  then,  should  the  patient  live,  imvproe- 
ment  slowly  sets  in.  In  some  cases  evidences  of  extension  upward  or 
downward  occur  (ascending  or  descending  myelitis) ;  the  symptoms  be- 
come more  severe,  and  in  a  few  weeks,  or  oftener  months,  death  occurs 
directly  from  bronchopneumonia  or  pyonephrosis. 

As  improvement  begins,  a  return  of  sensation  is  first  noticed  (one  to 
six  months);  this  is  followed  by  return  of  more  or  less  motion  (six  to 
eighteen  months).  Spasms  and  contractures  now  develop,  owing  to 
secondary  degenerations.  A  certain  amount  of  ataxia  from  posterior 
column  degeneration,  with  a  little  anaesthesia  of  the  skin,  may  remain,  so 


Fig.  100. — Acute    diffuse    myelitis. 


that,  if  the  patient  has  sufficient  motor  power  to  walk  somewhat,  he 
presents  many  features  of  "ataxic  paraplegia." 

Some  additional  and  continued  improvement  may  be  expected  for 
from  one  to  two  years.  A  few  cases  get  almost  entirely  well.  The  major- 
ity become  more  or  less  paraplegic  and  bedridden,  in  which  condition 
they  are  regarded  as  cases  of  chronic  myelitis,  though  no  active  process 
exists. 

Pathology. — The  infection  of  the  spinal  cord  in  acute  exudative  types 
of  myelitis  is  believed  to  be  through  the  lymph  paths  of  the  nerves  and 
not  through  the  blood-vessels  (lymphogenous  myelitis).  In  the  more 
severe  hemorrhagic  and  in  the  purulent  types  it  is  a  vascular  infection 
(hematogenous).     The  early  changes  found  are  those  of  inflammation. 


DISEASES    OF    THE    SPINAL    CORD 


229 


hemorrhagic  extravasation  and  softening.  Often  it  is  impossible  to  say 
whether  the  primarj^  process  was  inflammatory  or  due  to  a  hemorrhage 
or  softening. 

Macroscopicalh' ,  the  cord  at  the  affected  part  appears  soft,  swollen, 
and  either  red  and  hypersemic  or  pale  and  anaemic.  In  rare  cases  no 
change  is  apparent  to  the  naked  eye.  In  later  stages  the  parts  are  white 
or  gray,  shrunken  and  hard.  The  cord  may  be  reduced  to  a  thin  shred. 
The  meninges  about  the  affected  parts  are  often  thickened,  inflamed,  and 
adherent. 

Microscopical^,  if  the  process  is  primarily  inflammatory  we  find 
intense  congestion,  distended  blood-vessels,  emigrated  white  blood-cells 


\ 


^^^^ 


Fig.  101. — Acute  hemorrhagic  myelitis. 


in  great  number,  especially  in  the  perivascular  spaces,  swollen  axis-cylin- 
ders and  oedematous  swelling  of  the  myelin  sheath,  red  blood-cells,  cells 
filled  with  fat  granules  known  as  compound  granular  corpuscles,  or  Gluge's 
corpuscles  (Fig.  100). 

When  the  infection  is  very  intense  the  hemorrhagic  process  is  more 
active  (Fig.  101). 

In  fatal  cases  inflammation  and  softening  continue;  fresh  areas, of 
cord  are  involved,  much  meningeal  exudation  takes  place  and  finally 
death  occurs.  The  process  may  in  very  rare  cases  be  still  more  acute, 
suppuration  and  abscess  occur,  and  here  death  ensues  in  two  or  three 
weeks. 


230  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  inflammatory  and  softening  processes  above  referred  to  are 
described  in  accordance  with  their  appearance  as  red  softening,  yel- 
low softening  or  white  softening.  A  form  of  so-called  inflammation, 
known  as  inflammatory  oedema,  is  also  described.  It  is  an  abortive 
inflammation,  ''a  lymphatic  congestion,"  analogous  to  vascular 
congestion. 

The  diagnosis  of  acute  myelitis  must  be  made  from  hemorrhage, 
non-inflammatory  softening,  multiple  neuritis,  and  hysterical  or  func- 
tional paralysis.  Syphilitic  spinal  paralysis  (Erb's  type)  is  recognized 
by  the  cerebrospinal  fluid  tests.  Spinal  hemorrhage  comes  on  suddenly 
and  is  not  attended  by  fever.  If  meningeal,  it  is  attended  with  pain  and 
the  condition  soon  remits.  Acute  softening  not  syphilitic  usually  occurs 
only  in  old  people  with  spinal  arterial  sclerosis.  In  softening  there  is 
no  constitutional  disturbance,  no  leukocytosis,  the  process  is  slower, 
there  is  less  pain  and  the  dissociation  of  cutaneous  sensations  is  less 
marked.  In  acute  ascending  paralysis  the  disease  is  progressive,  there  are 
no  involvement  of  sensation,  no  atrophy,  and  little  change  in  the  electric 
irritability.  In  multiple  neuritis  the  onset  is  slower,  there  are  more  pain, 
local  tenderness  and  sensory  disturbance,  and  the  sensory  loss  is  of  the 
glove  and  stocking  types;  the  bladder  and  rectum  are  rarely  involved. 
In  meningitis  there  are  pain  and  tenderness  in  the  back  and  limbs,  rigid- 
ity, cramps,  a  little  paralysis,  and  no  bladder  trouble.  In  hysterical 
paraplegia  there  are  no  marked  atrophic  changes,  but  little  spasm  or 
rigidity,  no  electrical  changes,  and  the  stigmata  of  hysteria  may  be  found. 
The  sensory  disturbances  are  variable  and  somewhat  characteristic  (see 
Hysteria),  and  the  knee-jerks  are  not  greatly  if  at  all  exaggerated.  Tap- 
ping of  the  spinal  canal  will  enable  one  to  exclude  hemorrhage  and  to 
determine  by  the  presence  of  a  lymphocytosis  that  there  is  an  inflamma- 
tory process.  The  serological  tests  will  also  determine  whether  it  is  a 
syphilitic  process  or  not. 

The  diagnosis  of  the  location  of  the  lesion  is  made  by  studying 
the  height  of  the  anaesthesia,  the  skin  reflexes  (see  p.  46),  the  loss 
of  sphincter  control,  and  the  distribution  and  extent  of  the  paral- 
ysis. There  is  often  a  differentiation  of  the  ansesthesia,  as  shown  in 
Fig.  99. 

Prognosis. — The  prognosis  is  worse  the  more  complete  and  extensive 
the  paralysis.  It  is  worse  in  serious  motor  paralyses  than  when  sensa- 
tion is  chiefly  involved.  It  is  best  in  dorsal  myelitis  and  worse  usually  in 
cervical  myelitis,  other  things  being  equal.  Bed-sores  and  slight  fever  are 
unfavorable  signs;  so  also  is  severe  involvement  of  the  bladder  and  rec- 
tum. Recovery  of  sensation  gives  good  hope  of  recovery  of  some  motion. 
Total  absence  of  recovery  of  sensation  and  motion  after  six  months  is  very 
unfavorable.     Improvement  may  be  expected  up  to  eighteen  months  after 


THE    DISEASES    OF    THE    SPINAL    CORD  231 

the  onset,  and  in  some  cases  even  longer.  In  compression  myelitis  there 
is  more  chance  of  recovery  than  in  the  other  forms  provided  that  the  com- 
pressing agent  be  removed. 

Treatment. — In  the  attack,  the  patient  must  be  put  to  bed;  dia- 
phoresis should  be  promoted,  a  laxative  and  colon  washings  given,  and, 
in  general,  eliminative  treatment  followed.  Urotropin  and  small  doses 
of  aconite  and  nitroglycerin  may  be  prescribed.  The  bladder  should  be 
watched.  After  a  week,  moderate  doses  of  iodide  of  potassium  should 
be  given.  After  about  three  weeks,  if  there  is  no  fever,  electricity  may  be 
applied  carefully  and  strychnine  administered  in  small  doses.  Bed- 
sores should  be  guarded  against  by  the  use  of  water-beds,  or  cushions, 
absorbent  cotton,  bathing  the  parts  with  alcohol  and  weak  solutions  of 
tannin.  Infusion  of  buchu,  boric  acid  and  tincture  of  hyoscyamus  will 
often  help  the  bladder  disturbance.  Urotropin  and  sodium  benzoate 
may  be  also  needed.  The  frequency  of  syphilis  as  a  cause  of  acute 
paraplegia  (nearly  one-half  the  cases)  should  lead  to  the  persistent 
use  of  medication  for  this  condition  if  indicated.  After  acute  symptoms 
subside,  the  treatment  is  that  for  chronic  myelitis. 

CHRONIC  MYELITIS  AND  SOFTENING 

{Transverse  and  Com'pression  Myelitis,  ErVs  Syphilitic  Spinal 

Paralysis) 

Chronic  myelitis  is  the  name  given  to  a  disease  characterized  by  a 
chronic  inflammation  of  the  spinal  cord  and  to  the  chronic  reparative 
processes  which  follow  acute  inflammation,  injury  and  softening.  Chronic 
myelitis  is  usually  a  mixture  of  inflammatory,  reparative  and  necrotic 
processes  and  may  be  only  the  terminal  stage  of  acute  inflammation  or 
softening. 

Forms. — Different  names  are  given  to  chronic  myelitis  in  accordance 
with  the  part  of  the  cord  affected.  Usually  the  disease  affects  only  cer- 
tain levels,  and  then  it  is  called  transverse  myelitis.  More  rarely  it  is 
diffuse  or  disseminated,  central  or  marginal.  When  caused  by  pressure 
from  vertebral  disease,  it  is  called  compression  myelitis,  though  this  is 
really  often  only  an  inflammatory  oedema  secondary  to  a  peri-pachy- 
meningitis. 

Etiology. — The  disease  may  be  either  primary  or  secondary.  The 
primary  form  is  somewhat  the  rarer.  It  occurs  chiefly  in  adults  and  in 
early  and  middle  life,  and  much  oftener  in  males,  and  it  is  due  to  syphilis. 
Secondary  chronic  myelitis  is  a  rather  common  form.  It  is  really  only 
the  later  stage  of  acute  myelitis,  softening,  destructive  hemorrhages 
and  injuries. 


232  DISEASES    OF    THE    NERVOUS    SYSTEM 

Meningitis  may  extend  and  cause  a  meningomyelitis.  A  neuritis  may 
possibly  ascend  and  cause  myelitis,  but  such  cases,  if  they  occur  are  very 
rare.  When  all  is  said,  chronic  myelitis  as  usually  seen  is  a  syphilitic 
myelitis,  or  the  result  of  injury,  of  hemorrhage,  or  of  vertebral  caries. 

Among  67  personal  cases  of  secondary  chronic  myelitis  there  were 
61  men  and  6  women.  The  causes  that  can  be  assigned  were:  Syphilis, 
23;  injuries,  12;  exposure,  3;  acute  infection,  6,  of  which  3  followed 
grip,  1  typhoid,  1  meningitis,  and  1  mumps.  Two  were  due  to  caisson 
disease;  4  were  of  arteriosclerotic  origin  occurring  in  the  aged  and 
6  were  due  to  tuberculosis.  A  study  of  the  age  shows  that  practically 
all  the  cases  occur  between  the  ages  of  twenty-one  and  fifty,  and 
most  of  them  between  the  ages  of  thirty-one  and  forty.  Those  cases 
occurring  in  the  extreme  of  life  are  due  to  senile  arterial  changes  or 
injury. 

Symptoms  of  Primary  Chronic  Myelitis. — When  the  disease  begins 
primarily  as  a  chronic  affection  the  symptoms  are  as  given  below.  And 
since  nearly  all  such  cases  are  of  syphilitic  origin,  the  description  of  pri- 
mary chronic  myelitis  is  practically  that  of  syphilitic  spinal  paralysis 
(Erb's  spinal  paralysis). 

The  patient  notices  that  his  legs  seem  heavy  and  easily  get  tired; 
prickling  and  numb  sensations  are  felt  in  the  feet;  occasionally  a  little 
pain  develops  in  the  back  or  there  is  a  sense  of  constriction  about  the 
trunk.  The  legs  are  stiff,  and  tests  often  show  that  the  reflexes  are 
exaggerated,  with  ankle  clonus  and  extensor  response  (sign  of  Babinski). 
There  is  but  little  wasting  of  them,  however.  The  sexual  power  declines; 
the  bladder  gives  some  trouble,  there  being  a  tendency  to  retention;  the 
bowels  are  constipated.  After  a  few  weeks  or  months  there  is  a  partial 
paraplegia,  with  rigidity  of  the  limbs  and  exaggerated  reflexes.  Some 
anaesthesia  exists,  and  occasional  pain,  which  is  not  severe  and  is  felt  more 
in  the  back  than  the  legs.  Sensory  loss  is  usually  shght  compared  to  motor 
loss. 

The  muscles  have  later  wasted  somewhat,  but  show  no  decided  changes 
to  the  electrical  current.  The  bladder  becomes  more  involved,  the  urine 
has  to  be  drawn,  it  is  often  alkaline,  and  unless  care  is  taken  cystitis 
develops.  The  patient  is  still  able  to  walk,  but  he  does  so  with  a  stiff, 
shuffling  gait  which  is  characteristic  (Fig.  102).  The  disease  may  show 
signs  of  slowly  extending  up  and  down,  more  often  up.  The  arms  become 
involved;  weakness  and  stiffness,  with  some  wasting,  anaesthesia  and  pain, 
develop,  or  the  disease  may  cease  its  progress  and  the  patient  remain 
partly  paralyzed  for  years.  The  general  health  during  the  course  of  the 
disease  deteriorates  slowly;  the  patients  often  become  anaemic  and  have 
an  unhealthy  pallor.     Eventually  the  paraplegia  may  become  complete, 


THE    DISEASES    OF    THE    SPINAL    CORD 


233 


the  patient  is  bedridden,  the  legs  are  atrophied,  contractured  and  rigid, 
with  more  or  less  anaesthesia.  Cystitis  and  nephritis  develop,  and  the 
patient  dies  from  these  or  other  intercurrent  diseases. 

Chronic  secondary  myelitis,  which  is  the  form  often  seen,  presents 
eventually  much  the  same  picture  as  that  just  described.  In  this  type, 
however,  the  symptoms  are  those  of  an  acute  myelitis  first,  then  improve, 
then  become  stationary,  and  finally  grow  worse. 

Chronic  compression  myelitis,  so  called,  is  usually  only  a  compression 
oedema  with  partial  atrophy.  It  is  due,  as  a 
rule,  to  vertebral  caries  and  pachymeningitis, 
but  its  cause  may  be  a  spinal  tumor  or  aneurism. 
Compression  myelitis  is  distinguished  from 
other  forms  by  its  slow  onset  and  the  presence 
at  first  of  irritative  or  "root"  symptoms.  The 
patient  suffers  from  pain  and  tenderness  local- 
ized at  a  certain  point  in  the  spine.  The  pain 
radiates  about  the  trunk  or  down  the  limbs  and 
is  increased  on  movements.  At  about  the  same 
time  some  motor  weakness  develops,  usually 
in  the  form  of  paraplegia,  one  leg  being  often  af- 
fected some  weeks  or  months  before  the  other. 
The  muscles  waste  but  slightly.  The  reflexes 
are  exaggerated;  twitchings,  spasms  and  con- 
tractures finally  occur,  and  there  is  developed 
a  spastic  paraplegia  or  quadruplegia.  With 
this  there  is  usually  some  anaesthesia,  though 
it  is  not  complete.  The  disease  is  oftenest  in 
the  dorsal  or  lower  cervical  region,  and  hence 
the  sphincters  escape  until  late.  Ijocally,  evi- 
dences of  spine  disease  may  appear  early  in 
the  form  of  a  kyphosis. 

A  central  or  peri-ependymal  myelitis  can  rarely  be  recognized  with 
certainty.  It  produces  less  pain  and  irritation,  but  leads  to  muscular 
atrophy,  disorders  of  sensations,  such  as  thermo-ansesthesia,  disturbance 
of  vasomotor  and  secretory  nerves  and  visceral  centres. 

Pathology. — The  pia  mater  is  thickened  over  the  affected  region 
and  often  throughout  the  cord.  The  cord  itself  has  a  gray,  discolored 
look  at  the  affected  level,  and  is  usually  shrunken  or  distorted  and  hard  to 
the  touch.  In  severe  cases  of  secondary  character  it  is  reduced  to  a  small 
size,  and  the  membranes  about  it  are  thick  and  inflamed.  In  transverse 
myelitis  a  vertical  area  of  only  two  or  three  inches  is  involved.  The 
microscope  shows  that  the  prominent  changes  are  loss  of  nerve  struc- 
ture, great  increase  of  connective  tissue  and  increase  in  the  number 


Fig.  102. — Chronic  myelitis. 


234  DISEASES    OF    THE    NERVOUS    SYSTEM 

of  vessels,  which  often  have  thickened  walls.  In  the  more  seriously 
diseased  part  little  is  seen  but  connective  tissue.  In  parts  less  diseased 
some  nerve-fibres  are  seen,  many  having  evidences  of  partial  disintegra- 
tion. There  is  also  a  good  deal  of  amorphous  material  studded  with 
nuclei.  Stellate  cells,  granule  cells,  and  nerve-cells  in  various  stages  of 
degeneration  are  present.  In  the  parts  less  affected  the  signs  of  con- 
gestion and  vascular  irritation  are  more  pronounced.  Secondary 
degenerations  occur  above  and  below  the  seat  of  the  myelitis  (Figs.  113 
and  114).  In  the  typical  syphilitic  myelitis  the  meninges  are  thickened 
and  there  is  a  predilection  for  the  inflammatory  change  to  affect  the 
lateral  columns  of  the  cord  (Fig.  103). 


Fig.  103. — Syphilitic  meningo-myelitis ;  cervical  region. 

Diagnosis. — This  must  be  made  from  progressive  muscular  atrophy 
and  amyotrophic  lateral  sclerosis,  pachymeningitis  and  spinal  tumor; 
from  locomotor  ataxia,  multi'ple  sclerosis  and  brain  palsies. 

In  progressive  muscular  atrophy  there  is  a  peculiar  atrophy  without 
involvement  of  the  sphincters  or  sensory  disturbance.  Tumors  usually 
cause  much  more  pain;  the  symptoms  come  on  slowly  and  are  more  uni- 
lateral at  first  and  more  definitely  localized.  A  spastic  paraplegia  occurs 
in  cerebral  diplegia,  but  the  arms  are  also  sometimes  involved,  and 
there  are  no  trophic  or  sensory  troubles,  nor  is  there  involvement  of 
the  sphincters.  In  locomotor  ataxia  there  is  no  great  degree  of  motor 
paralysis,  and  there  are  peculiar  ataxic  and  sensory  disturbances.  In 
the  early  stages  of  multiple  sclerosis  of  the  spinal  type,  however,  the 
symptoms  resemble  closely  a  very  slowly  developing  chronic  myelitis. 
The  diagnosis  can  be  made  by  remembering  that  in  multiple  sclerosis 
patient  is  usually  young,  that  there  is  absence  of  much  sensory  trouble,  and 


THE    DISEASES    OF    THE    SPTXAL    CORD  235 

presence  upon  close  examination  of  e3-e  trouble,  tremor,  speech  dis- 
turbance and  paresthesias  in  multiple  sclerosis  the  course  is  often  a  remit- 
ting one,  the  abdominal  reflexes  are  usualh'  lost  and  the  bladder  be- 
comes affected  quite  early.  Paralysis  from  brain  disease  is  almost  alwaj'-s 
unilateral,  painless,  spastic  and  free  from  disturbance  of  the  visceral 
centres. 

Prognosis. — Inflammatory  processes  have  a  tendency  to  cease  when 
their  reparatoiy  and  eliminative  work  is  done.  And  this  is  true  of 
mj-elitis.  However,  in  the  spinal  cord  secondary  degenerations  set  in 
as  soon  as  certain  tracts  are  interfered  with.  Hence  chronic  myelitis, 
after  a  period  of  improvement,  generally  progresses,  and  the  prognosis 
is  not  ver}-  favorable.  Still,  patients  may  live  comfortabh^  from  five 
to  twenty-five  years.  Dorsal  myelitis  is  the  most  favorable  form; 
compression  myelitis  from  caries  can  also  often  be  successful!}'  treated. 
Syphilitic  myelitis  and  meningomyelitis  unless  treated  are  liable  to  take 
a  progressive  course,  Hke  a  locomotor  ataxia.  Serious  involvement  of 
the  bladder  is  a  bad  sign,  and  naturally  the  prognosis  is  worse  the  more 
complete  the  paralysis. 

Treatment. — In  the  treatment  of  chronic  myelitis  the  cause  must  be 
sought  and  treatment  applied  accordingly.  If  it  is  sj'philis  a  thorough- 
going course  of  anti-s^'philitic  measures  should  be  instituted. 

If  it  is  a  compression  myelitis  from  Pott's  disease,  prolonged  rest  in  bed 
for  six  months  or  more  is  usually  adequate.  Jackets  and  various  forms  of 
support  are  helpful  but  alone  are  not  enough. 

If  the  cause  is  caisson  disease,  injury  by  fracture  or  wounds,  rest 
and  mechanical  measures  are  the  essential  things. 

Various  supplementary  and  symptomatic  measures  are  to  be  used. 
Counterirritation  in  the  form  of  fly-blisters,  or  the  cautery,  may  be  ap- 
plied and  wet  or  dry  cups  used.  The  descending  galvanic  current  along 
the  spine  should  be  tried;  faradism  and  massage  being  used  upon  the  limbs. 
Lukewarm  baths.  90°  to  98°F..  or  half-baths  with  frictoin  at  70°  to  80°F., 
are  likely  to  be  useful,  but  these  must  be  tried  cautiously.  The  first 
baths  should  last  not  over  five  minutes  and  should  be  repeated  only  three 
or  four  times  weekly.  In  later  paraplegic  and  bedridden  stages,  electrical 
and  hydrotherapeutic  apphcations  should  be  followed  up  patiently  and 
persistentl}^  The  patient  may  be  allowed  to  remain  and  exercise  in  the 
lukewarm  bath  for  some  time.  The  patient  may  be  given  courses  of 
tonic  treatment,  using  phosphates,  iron,  arsenic,  and  small  doses  of 
strychnine.  The  more  surelj'  the  disease  is  non-luetic,  the  more  are 
simple  tonic  and  mechanical  measures  alone  indicated.  For  the  bladder 
troubles,  the  internal  use  of  boric  acid,  belladonna,  ergot  buchu,  and 
urotropin  are  helpful.  Salvarsan  is  of  little  or  no  value  in  long-standing 
chronic  mj-elitis,  unless  the  disease  is  progressing. 


236  DISEASES    OF    THE    NERVOUS    SYSTEM 

ACUTE  POLIOMYELITIS 

(Epidemic  Poliomyelitis;  Infantile  Paralysis) 

This  disease  results  from  an  infection  of  the  body  by  a  specific  organ- 
ism, which  produces  acute  constitutional  symptoms  of  a  reactive  char- 
acter; this  organism  has  an  especial  affinity  for  the  central  nervous  sys- 
tem, whereby  it  usually  produces  an  acute  flaccid  motor  paralysis,  in 
muscles  segmentally  grouped  which  subsequently  undergo  more  or  less 
atrophy. 

Etiology. — It  occurs  at  all  ages,  but  60  per  cent,  of  the  cases  are  in 
children  under  three  years.  About  15  per  cent,  of  the  cases  are  in 
adults  usually  under  thirty. 

The  disease  occurs  epidemically  and  to  a  lesser  extent  sporadically. 
Almost  all  the  cases  appear  in  the  summer  months,  especially  in  August 
and  September.  Epidemics  occur  rather  more  often  on  the  coast  board 
and  in  low-lying  places;  the  principal  epidemics  described  have  been  in 
Scandanavia  from  1903  to  1906,  Minnesota,  New  York  1907  and  1908, 
Victoria,  Australia  1907,  Massachusetts  1908,  Vienna  1908.  Smaller  epi- 
demics have  been  reported  from  various  parts  of  France,  England  and 
the  United  States.  No  specific  cause  can  be  cited  as  rendering  the  body 
liable  to  attack;  all  factors  lowering  vital  resistance  are  probably  contribu- 
tory to  infection,  such  as  malnutrition,  fatigue,  and  other  infectious  dis- 
eases.    The  incubation  period  varies,  but  averages  ten  days  in  length. 

Bacteriology. — In  the  summer  of  1909  Landsteiner  and  Popper  suc- 
ceeded in  producing  the  disease  in  two  monkeys  by  intra-peritoneal  injec- 
tion of  emulsified  spinal  cord  obtained  from  a  fatal  case  of  poliomyelitis. 
They  failed,  however,  to  transmit  the  disease  from  these  to  other  monkeys. 
In  September  of  the  same  year  Lewis  and  Flexner  working  at  the  Rocke- 
feller Institute  also  succeeded  in  producing  the  disease  in  monkeys  by 
means  of  intra-cerebral  injection  of  poliomyelitic  cord.  The  cords  of 
the  affected  monkeys  furnished  a  virus  which  by  September  1910  had 
been  propagated  through  twenty-five  separate  series  of  monkeys.  The 
virus  is  found  to  pass  readily  through  a  Berkefeld  or  Chamberland  filter. 
It  withstands  glycerinization,  drying  and  freezing  over  prolonged  periods, 
but  is  readily  destroyed  by  heat  and  by  comparatively  weak  antiseptics 
such  as  menthol  and  a  1  per  cent,  solution  of  hydrogen  peroxide.  In 
1913  the  virus  was  cultivated  with  difficulty  by  Flexner  and  Noguchi 
under  anaerobic  conditions;  subcultures  in  the  fifth  generation  have  suc- 
cessfully reproduced  the  disease  in  monkeys.  The  minute  colonies  are  com- 
posed of  globular  bodies  averaging  0.15  to  0.3  micron  in  size;  these  occur 
in  short  chains,  in  pairs,  and  in  masses,  and  are  stainable  by  Giemsa's 
or  Gram's  methods.  The  virus  can  be  inoculated  with  success  into  the 
brain;  into  the  subdural  space;  subcutaneously;  by  introduction  into  the 


THE  DISEASES  OF  THE  SPINAL  CORD 


237 


stomach  and  into  the  intestines.  It  has  been  shown  that  it  can  be  carried 
from  the  ill  to  the  well  through  the  intermediate  agencies  of  the  house 
fly,  the  stable  fly,  Stomoxys  calcitrans,  and  the  bedbug.  Experiments 
directed  to  prove  an  identical  role  on  the  part  of  mosquitoes  and  lice 
were  negative.  Flexner  and  Amoss,  however,  in  papers  published  in 
1914  believe  that  infection  is  local  and  by  way  of  the  lymphatics,  and 
not  general  and  by  way  of  the  blood.  They  believe  the  virus  enters  the 
body  through  the  nasopharyngeal  mucous  membrane,  and  hence  through 
the  lymphatics  of  the  olfactory  nerve  to  the  leptomeninges.  An  attack 
of  poliomyelitis  confers  an  active  immunity  against  a  second  infection. 
This  obtains  apparently  for  at  least  three  years.  Successful  vaccination 
against  the  virus  has  been  achieved  in  the  macacus  but  not  as  yet  in  man. 
It  has  been  shown  experimentally  that  the  previous  administration  of 


Fig.  104. — Acute  anterior  poliomyelitis  showing  diffusely  inflamed  area  on  right  side. 

urotropin  will  in  the  monkey  increase  the  incubation  period  of  the  in- 
oculated disease  and  diminish  its  severity. 

Pathology. — Naked-eye  appearances :  The  brain  may  be  oedematous 
and  show  some  vascular  engorgement.  The  cord  also  may  be  oedematous 
with  some  wrinkling  of  the  swollen  and  congested  meninges.  On  section 
the  distinction  between  gray  and  white  matter  may  be  diminished  through 
softening  especially  in  the  severely  affected  areas,  usually  the  cervical 
and  lumbar  enlargements.  Similar  softenings  may  be  found  in  the  brain 
stem  or  hemispheres.  The  spleen  is  enlarged  and  changes  varying  from 
coagulation  to  hemorrhage  may  be  found  in  the  kidneys  and  liver.  The 
microscopic  lesions  in  the  brains  and  cords  of  fatal  cases  consist  mainly 
of  congestion  and  hemorrhage  into  the  gray  matter;  the  anterior  horns 
being  disproportionately  affected.  The  entire  spinal  cord  may  be  in- 
volved in  a  series  of  vascular  accidents  of  varying  degree.     The  lesions 


238  DISEASES    OF    THE    NERVOUS    SYSTEM 

consist  of  a  small  round-celled  infiltration  in  the  perivascular  spaces  with 
the  development  of  considerable  oedema.  Arterial  thrombosis  is  never 
apparent,  and  the  degeneration  and  necrosis  of  cells  are  invariably  pro- 
duced by  gross  pressure  of  inflammatory  exudates  on  the  cells  and  the 
nutrient  blood-vessels.  A  leptomeningeal  infiltration  of  mononuclear 
cells  is  always  present  and  is  perivascular  in  position.  The  greater  affec- 
tion of  the  anterior  over  the  posterior  horns  is  explicable  by  the  richness 
of  the  vascular  supply  to  the  former;  a  similar  consideration  serves  to 
explain  the  apparently  disproportionate  involvement  of  the  lumbar  and 
cervical  enlargements  (Figs.  104,  105  and  106). 


Fig.  105. — Acute  anterior  poliomyelitis.     Same  as  previous  figure  enlarged,  showing 

loss  of  cells  in  right-horn. 

Signs  and  Symptoms. — These  may  be  conveniently  described  under 
different  headings :  (1)  A  prodromal  period — lasting  a  few  days;  (2)  an 
acute  stage  of  a  few  hours  to  a  week;  (3)  a  stationary  period — one  to  six 
weeks,  usually  two  weeks;  (4)  a  stage  of  improvement — six  months  to 
three  or  four  years;  (5)  a  chronic  stage  of  residual  incurable  atrophic 
palsy. 

1.  In  some  cases  the  onset  of  the  acute  stage  is  so  rapid  that  the  pro- 
dromal period  is  practically  eHminated,  but  the  vast  majority  of  patients 
complain  of  some  general  malaise,  and  headache  of  considerable  severity 
with  occasional  vomiting.  Drowsiness  combined  with  irritability  is 
usually  present.    There  is  generalized  hyperaesthesia  with  pain  in  the  back, 


THE    DISEASES    OF    THE    SPINAL    CORD 


239 


in  the  neck  muscles — which  may  also  be  rigid,  and  in  the  limbs;  the  pain  is 
usually  greatest  in  limbs  subsequently  paralyzed.  Constipation  is  usual; 
there  are  present  much  generalized  sweating  and  a  moderate  fever  and 
leukocytosis  in  blood  and  spinal  fluid. 

2.  The  constitutional  symptoms  of  the  prodromal  period  may  be 
carried  on  through  the  few  hours  or  days  of  the  second  stage  in  which 
motor  paralyses  appear.  These  come  suddenly  and  achieve  their  maxi- 
mum severity  within  a  few  hours.  The  affected  limbs  are  toneless  and 
tender.  Sensory  changes  are  very  rare  and  transient.  Sphincter  dis- 
turbance is  usual  but  quickly  passes.  The  paralysis  most  often  affects 
both  legs,  next  one  leg,  next  the  arms  and  legs,  and  after  this  various 


Fig.  106. — Acute  anterior  poliomyelitis. 


combinations.  The  cranial  nerve  nuclei  may  be  attacked,  and  in  the  not 
very  common  cases  where  the  cerebrum  is  affected  there  may  result 
hemiplegia  of  upper  motor  neurone  type  with  some  residual  intellectual 
impairment.  The  term  polioencephalitis  superior  has  been  apphed  to 
those  cases  where  the  oculomotor  nuclei  are  destroyed;  affection  of  the 
nuclei  placed  lower  in  the  brain  stem  has  been  called  polioencephalitis 
inferior.  Cases  in  this  stage  prove  fatal  usually  from  medullary  in- 
volvement or  paralysis  of  the  respiratory  muscles. 

3.  The  paralysis  remains  at  its  height  for  from  one  to  six  weeks,  and 
then  improvement  gradually  sets  in.  In  two  or  three  weeks  a  wasting 
of  the  paralyzed  limb  may  be  noticed.     It  is  flabby,  its  temperature  is 


240 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


lowered,  and  the  reflexes  may  be  gone.     Slight  tenderness  may  be  present 
but  there  is  no  anaesthesia. 

4.  The  stage  of  improvement  lasts  for  from  six  months  to  several 
years.  The  paralysis  gradually  disappears,  beginning  in  the  limbs  least 
injured.  This  continues  until  but  one  or  two  limbs  are  still  affected. 
In  them  the  muscles  are  wasted  and  show  the  reaction  of  degeneration, 
viz.,  loss  of  faradic  irritability,  retention  and  slowing  of  galvanic  irrita- 
bility, and  sometimes  polar  changes.  In  the  leg,  the  anterior  tibial  and 
peroneal  groups  are  oftenest  affected;  in  the  arm,  the  muscles  of  the  shoul- 
der girdle.  After  eighteen  months  not  much  further  spontaneous  im- 
provement can  be  expected,  but  much 
can  usually  still  be  done  by  vigorous 
massage  and  suitably  adapted  exercises. 
5.  The  temperature  of  the  affected 
limbs  is  lowered  several  degrees;  the 
skin  has  a  reddish-purplish  mottled 
look.  The  bones  as  well  as  the  mus- 
cles of  these  limbs  do  not  grow  as  well 
as  those  of  the  others.  Hence  in  time 
the  extremity  is  disproportionately 
small  and  short  (Fig  108).  Owing  to 
the  contraction  of  unopposed  muscle 
deformities  occur.  The  most  frequent 
are  talipes  equinus,  talipes  varus  and 
valgus.  Deformities  of  the  knees,  and 
contraction  of  the  plantar  fascia  also 
take  place.  Spinal  curvature  is  com- 
mon in  cases  in  which  the  supporting 
back  muscles  have  been  affected.  The 
general  health  of  the  patient  is  usually 
good.  A  consideration  of  the  path- 
ology of  this  disease  will  make  evident  the  fact  that  many  different 
clinical  varieties  must  occur  to  correspond  with  the  varied  combinations 
of  spinal  and  cerebral  lesions  produced 

The  following  distinct  types  may  be  mentioned: 

1.  Spinal  poliomyelitis — a  sudden  feverish  attack  followed  by  the 
palsy  of  one  or  more  limbs. 

2.  An  ascending  form  in  which,  first,  are  involved  the  legs  and  later 
the  abdomen  and  thorax.     This  type  is  often  fatal. 

3.  A  bulbar  type,  with  palsies  of  the  various  pontine  and  medullary 
cranial  nerve   nuclei. 

4.  Polioencephalitis,  from  which  a  state  of  meningismus  with  spastic 
paralyses  may  ensue. 


Fig.  107. — ^Poliomyelitis,  late  stage 
showing  atrophied  and  shortened  leg. 
(Schoenborn  and  Krieger.) 


THE    DISEASES    OF    THE    SPINAL    CORD  241 

5.  Ataxic  polioencephalitis,  by  which  is  merely  meant  a  specific 
inflammatory  process,  the  maximum  stress  of  which  falls  on  the  cerebellum. 
The  clinical  symptoms  are  briefly,  an  acute  illness  of  short  duration,  fol- 
lowed by  motor  ataxia  of  the  arms  and  legs,  nystagmus,  and  explosive 
syllabic  speech. 

6.  Abortive  forms  in  which  only  general  constitutional  disturbances 
occur,  and  paralyses  are  either  cjuite  fleeting,  or  entirely  absent.  In 
these,  diagnosis  may  be  surmised  from  the  co-existence  of  an  epidemic  of 
the  disease,  and  confirmed  by  spinal  fluid  examination.  The  necessity  of 
making  correct  diagnoses  in  these  cases  is  indicated  by  the  fact  that  polio- 
myelitis has  been  propagated  through  successive  series  of  animals,  from 
the  nasal  washings  of  an  abortive  case. 

Diagnosis. — The  initial  symptoms  of  poliomj-elitis  are  almost  gen- 
eric for  all  infected  conditions.  Influenza  must  be  thought  of.  Against 
it  one  puts  the  seasonal  unlikelihood,  it  being  a  winter  and  spring  disease. 
In  poliomyelitis,  catarrhal  sjanptoms  will  be  absent.  Gastroenteritis  is 
most  frequent  in  the  summer  and  early  autumn,  but  in  it  the  onset  is 
less  rapid,  pyrexia  less  sudden,  while  somnolence,  general  hypersesthesia, 
and  sweating  are  infrequent.  Constipation  rather  than  diarrhoea  obtains 
in  the  early  stages  of  the  cord  affection.  Lumbar  puncture  should  be 
performed  early  in  all  doubtful  cases,  particularly  to  differentiate  the  con- 
dition from  tuberculous  and  diplococcal  meningitis.  The  main  char- 
acteristics of  the  three  fluids  may  be  here  contrasted : 

Tuberculous  meningitis:  Clear,  forming  a  fine  clot  on  standing. 
Globulin  content  early  increased.  The  normal  reduction  of  Fehling's 
solution  often  lost.  Usually  an  almost  pure  Ijaiipocytosis  from  the 
very  beginning  of  the  disease.  In  85  per  cent,  tubercle  bacilli  may  be 
demonstrated. 

Diplococcal  meningitis:  Fluid  turbid  and  heavily  albuminous. 
Fehling's  test  positive  except  in  very  chronic  cases.  Almost  pure 
polymorph  leukocytosis.  Gram-negative  diplococci  may  be  easily 
demonstrated.     (See  also  "Cerebro-spinal  Meningitis".) 

Acute  poliomyelitis:  Fluid  clear.  Clot  formation  on  standing  slight. 
Globulin  content  slightly  raised  in  early  stages,  and  gradually  rises  for 
about  three  weeks  after  which  it  may  sink  to  normal.  Fehling's  test 
normal.  In  the  first  three  days  of  the  disease  there  is  usually  an  almost 
pure  polymorph  leukocytosis,  as  high  as  1,000  per  cubic  millimeter.  This 
is  then  replaced  by  an  almost  pure  lymphocytosis  of  gradually  diminishing 
severity.  No  organisms  can  be  demonstrated  by  ordinary  methods. 
The  disease  must  also  be  distinguished  from  toxic  polyneuritis,  birth  pal- 
sies and  progressive  muscular  atrophy.  A  consideration  of  the  following 
facts  will  usually  make  the  diagnosis  easy: 

1.  The  age  of  the  patient. 

16 


242 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


2.  The  presence  of  an  epidemic  of  poliomyelitis  and  its  seasonal 
variations. 

3.  The  abrupt  onset  and  rapid  development  of  extreme  paralysis. 

4.  The  tendency  to  improve. 

5.  The  segmental  character  of  the  paralysis;  the  absence  of  bladder 
disturbance  and  objective  sensory  losses. 

Prognosis. — The  patient  rarely  dies,  either  from  the  disease  or  its 

sequelae.  In  some  epidemics,  however, 
there  has  been  a  mortality  of  about  12 
per  cent.  He  always  improves,  but  he 
recovers  completely  in  only  a  small  num- 
ber of  cases.  In  these,  no  cell  necrosis  has 
occurred  but  only  cell  deterioration. 

Treatment. — The  patient  should  be 
isolated  in  an  airy  room,  the  windows  of 
which  are  well  screened.  Faeces,  urine 
and  nasopharyngeal  discharges  must  be 
rendered  inocuous  by  antiseptics  as  in  a 
case  of  typhoid  fever.  A  nasal  spray  of  1 
per  cent,  hydrogen  peroxide  must  be  used 
and  maintained  for  some  months.  Uro- 
tropin  must  be  given  immediately  and 
maintained  in  large  doses  for  at  least  two 
weeks.  All  persons  exposed  to  poliomye- 
litic  infection  should  be  encouraged  to  use 
antiseptic  nasal  sprays  and  should  be 
given  urotropin  gr.  v.  twice  daily  as  a 
prophylactic  measure.  Rest  is  essential. 
The  bowels  should  be  opened  and  a  diu- 
retic given  (calomel  gr.  ii. ;  tartrat.  potas, 
gr.  XX.).  Lumbar  puncture  will  aid  diag- 
nosis  and   relieve,   at  least   temporarily, 

Fig.     108. — Poliomyelitis,   late  spinal  congestion.     Sedatives  may  be  re- 
stage,  showing  atrophy  of  leg  and         •     j  •     j.u  i       j.  a-*-        t ;^^  ,•„ 

deformity  of  foot.    {Schmibornand  qmred  m  the  early  stages.     Strychnme  is 

Krieger.)  to  be  avoided.     A  hot  pack  twice  a  day  will 

relieve  tenderness.  Aconite  and  sweet 
spirits  of  nitre  may  be  given  to  reduce  fever.  The  limbs  should  be 
wrapped  in  cotton  and  defended  from  pressure.  When  hypersensitive- 
ness  has  disappeared  gentle  massage  and  passive  movements  should  be 
instituted,  for  from  five  to  twenty  minutes  five  or  six  times  a  day.  Elec- 
trical applications  should  be  begun  cautiously,  at  first  three  times  a  week 
and,  when  well  borne,  daily.  Frequent  systematic  rubbings  given  by  a 
relative  are  frequently  more  productive  of  good  results  than  are  less 


THE    DISEASES    OF    THE    SPINAL    CORD  243 

frequent  treatments  given  by  a  trained  masseuse.  The  child  must  be 
trained  to  try  to  use  the  hmb  as  much  as  possible :  with  this  in  view  it  is 
inadvisable  to  keep  the  patient  confined  to  bed  after  the  acute  stage  has 
passed :  the  child  should  be  laid  on  a  well-blanketed  floor  and  encouraged 
to  crawl  and  push  its  way  about  the  room.  For  older  children  and 
adults  much  can  be  done  by  the  studious  performance  several  times  daily 
of  exercises  adapted  to  develop  the  affected  muscles  and  those  adjacent  to 
them.  Generally  speaking,  it  is  a  mistake  to  employ  orthopaedic  appa- 
ratus until  two  years  have  passed,  nor  should  they  be  employed  even  then 
unless  it  be  clear  that  developmental  exercises  are  useless.  The  same 
attitude  should  be  adopted  toward  operations  for  the  correction  of  deformi- 
ties or  for  restitution  of  function  by  nerve  grafting ;  such  procedures  are 
often  of  the  greatest  value  but  must  only  be  employed  after  much  con- 
sideration in  selected  cases.  Foster  Kennedy. 

CHRONIC  ANTERIOR  POLIOMYELITIS 

{Remitting  Spinal  Amyotro'phy) 

This  disease  goes  under  the  name  of  chronic  poliomyelitis,  but  it 
shows  a  closer  relation  to  obliterative  vascular  disease,  than  to  a  simple 
inflammatory  process. 

Etiology. — In  my  experience  syphilis  has  always  been  present;  others 
give  as  causes  lead,  overwork,  exposure  and  trauma.  It  occurs  only  in 
adults  and  in  men  more  than  women. 

Symptoms. — The  disease  comes  on  subacutely;  that  is  to  say,  in  one 
or  two  months.  It  reaches  its  height  in  three  or  four  months  and  before 
the  end  of  a  year  has  come  to  a  standstill.  The  symptoms  then  usually 
remain  quiescent  or  improve  for  one  or  two  years,  then  take  a  fresh 
start  and  present  about  the  same  course,  involving  new  and  usually 
neighboring  groups  of  cells.  It  may  progress  no  further  after  this  second 
attack,  but  there  sometimes  occur  fresh  invasions  involving  finally  the 
bulbar  nuclei  and  leading  to  a  fatal  issue.  The  symptoms  of  paralysis 
or  weakness  precede  the  atrophy,  which  is  a  flaccid  one,  but  in  other 
respects  it  resembles  the  ordinary  spinal  amyotrophies.  There  are 
slight  or  no  symptoms  of  involvement  of  the  pyramidal  tracts.  There 
is  sometimes  slight  fibrillary  tremor.  The  cUsease  usually  affects  the 
upper  extremities  and  especially  the  shoulder  girdle,  but  eventually 
involves  the  forearms  and  ascends  to  the  cervical  region  (Figs.  109,  110). 

The  tendency  to  cessation  of  progress  and  even  to  improvement  has 
characterized  cases  reported  by  Eisenlohr,  and  Landouzy  and  Dejerine. 
Few  cases  with  autopsy  have  been  reported,  and  these  showed  vascular 
lesions  with  secondary  degeneration  of  the  anterior  horn  cells  and  some- 
times of  the  anterior  fundamental  column. 


244 


DISEASES    OF    THE    NERVOUS    SYSTEM 


The  Prognosis  in  the  past  has  been  uniformly  bad. 

Treatment. — The  history  of  syphihs  in  my  cases  leads  to  the  recom- 
mendation of  an  anti-syphilitic  treatment  for  this  trouble,  and  this  must 
be  very  active  and  persistent. 


Fig.  109.- 


-Chronic  anterior  poliomyelitis,  luetic  right  shoulder  and  left  forearm  and 
hand  are  most  affected. 


Senile  Paraplegia. — Paraplegia  sometimes  develops  in  the  senile  and 
does  so  in  a  somewhat  characteristic  manner. 

In  the  spastic  form  the  paralysis  comes  on  slowly,  the  legs  are  stiff,  the 
gait  shuffling,  the  steps  very  short  and  the  feet  are  barely  raised  from  the 
ground.  There  is  some  pain  in  the  back,  at  times,  but  no  marked  sensory 
symptom.  There  may  be  decrease  in  reflexes  or  no  change.  The  sphinc- 
ters are  not  involved.  The  gait  and  station  suggest  paralysis  agitans, 
and  some  cases  may  be  considered  a  symptomatic  type  of  this  trouble. 

A  paraplegia  spastica  senilis  described  by  Demange  and  Oppenheim 


THE    DISEASES    OF    THE    SPINAL    CORD 


245 


is  of  arteriosclerotic  origin  and  accompanied  with  signs  of  pyramidal  de- 
generation. 

In  the  flaccid  form  of  senile  paraplegia  the  patient  progressively  but 
intermittently  grows  weaker  in  the  legs,  the  muscles  waste,  the  gait  is 
feeble,  with  short  steps  and  great  difficulty  in  going  up  and  down  stairs. 
There  is  sometimes  lumbar  pain,  and  the  sphincters  may  be  involved. 
The  patients  sometimes  improve,  but  even- 
tually become  helpless,  though  the  prog- 
ress is  slow.  I  have  had  an  autopsy  in 
one  case  and  found  very  marked  arterio- 
sclerotic changes  in  the  anterior  horns  of 
the  lumbar  region  with  softening.  I  think 
that  in  flaccid  senile  paraplegias  and  some 
of  the  rigid  types  there  is  arterial  sclerosis 
of  the  anterior  vessels  with  softening  and 
at  times  small  hemorrhages  (Fig.  112). 

Starr  thinks  that  some  forms  of  pro- 
gressive senile  paraplegia  are  neuritic  and 
that  others  are  due  to  a  progressive  muscu- 
lar disease  (dystrophy) . 

ACUTE  ASCENDING  PARALYSIS 

(Landry's  Paralysis) 

Acute  ascending  paralysis  is  a  disease 
characterized  by  a  rapidly  [developing 
paralysis  which  begins  in  the  legs  and 
then  involves  in  turn  the  trunk,  arms, 
respiratory  and  throat  muscles,  usually- 
ending  in  death.  There  is  little  disturb- 
ance of  sensation,  no  atrophy  or  changes 
in  electrical  irritability,  and  no  involve- 
ment of  the  sphincters.  It  is  thought  to  be 
related  to  acute  anterior  poliomyelitis. 

"The    Heine- 


Wickmann    under   the    name 
Medin  disease"  groups  together: 

1.  Acute  poliomyelitis. 

2.  Landry's  paralysis. 

3.  Bulbar  and  pontine  forms. 

4.  Encephalitic  forms. 


Fig.  110. — Remitting  muscu- 
lar atrophy.  Patient  is  unable 
to  raise  the  head. 


5.  Ataxic  forms. 

6.  Polyneuritic  forms. 

7.  Meningitic  forms. 

8.  Abortive  forms. 


This  assumes  that  the  same  infectious  or  toxic  agent  may  attack  the  different 
parts  of  the  nervous  system.  This  is  practically  the  conception  taught  in  the  earlier 
editions  of  this  work.  However,  all  forms  of  acute  ascending  paralysis  as  it  is  seen 
clinically  are  not  due  to  the  poliomyelitic  organism. 


246 


DISEASES    OF    THE    NERVOUS    SYSTEM 


Etiology. — The  disease  is  a  rare  one.  It  occurs  chiefly  between  the 
ages  of  twenty  and  forty;  men  are  affected  oftener  than  women.  Ex- 
posure is  an  exciting  cause,  and  it  occurs  sometimes  after  acute  infectious 
fevers.  The  form  of  rabies  known  as  ''paralytic"  causes  a  disease  which 
is  apparently  identical  with  Landry's  paralysis.  The  form  which  is 
caused  by  the  micro-organism  of  anterior  poliomyelitis  occurs  naturally 
when  epidemics  of  this  disease  are  present.  It  is  not  yet  proved  that  true 
ascending  paralysis  is  always  poliomyelitic. 

Symptoms. — There  may  be  slight  premonitory  symptoms  for  a  few 
days,  consisting  of  numbness  in  the  extremities,  pain  in  the  back  or 
limbs  and  malaise.  The  first  definite  sign  of  the  disease  is  weakness  in 
the  legs,  which  rapidly  increases,  until  in  a  day  or  two  the  patient  cannot 
walk.     The  paralysis  soon  involves  the  trunk,  arms  and  the  muscles  of 


Fig.  111. — Lumbar  coid  m  a  case  of  senile  paiaplegia,  showing  atrophy  of  anterior 
cornua  secondary  to  vascular  disease. 


respiration;  the  medulla  is  last  affected,  and  then  respiration  becomes 
difficult;  swallowing  and  articulation  may  be  impossible.  In  rare  cases 
there  are  facial  and  eye  palsies.  During  the  course  of  the  paralysis  there 
is  little  pain  or  sensory  disturbance,  but  some  degree  of  anaesthesia  may 
occur.  The  deep  reflexes  are  aboHshed.  There  are  no  vasomotor  and 
no  secretory  disturbances,  no  noticeable  atrophy,  and  no  degenerative 
reactions  in  the  affected  muscles.  The  bladder  and  rectum  are  involved 
only  in  rare  cases.  There  may  be  slight  initial  fever,  but  none  occurs 
after  the  disease  has  well  set  in.     The  mind  remains  clear. 

The  disease,  as  a  rule,  ends  fatally,  and  it  usually  runs  its  course  in 
less  than  a  week.  Death  has  occurred  in  forty-eight  hours.  On  the 
other  hand,  death  has  been  postponed  three  or  four  weeks. 

In  other  cases  the  disease  stops  short  of  the  medulla.     The  patient 


THE    DISEASES    OF    THE    SPINAL    CORD  247 

becomes  totally  or  nearly  paralyzed  below  the  neck.  He  then  begins 
slowly  to  improve,  and  this  improvement  continues  for  one  or  two  j^ears. 
Eventually  a  fair  degree  of  health  is  obtained. 

Variations. — The  disease  has  been  known  to  begin  in  the  medulla  or 
cervical  region  and  descend. 

Pathological  Anatomy. — There  are  three  pathological  conditions 
which  may  cause  the  symptoms  of  acute  ascending  paralysis:  (1)  Acute 
poliomyelitis;  (2)  acute  high  transverse  myelitis;  (3)  acute  multiple 
neuritis.  These  different  conditions  may  coexist  at  times  in  the  same 
case.  Usually  as  stated  the  micro-organisms  of  epidemic  poHomyelitis 
anterior  are  the  cause.  In  some  cases  the  symptoms  are  due  to  paralytic 
rabies,  in  others,  the  streptococcus,  the  diplococcus  and  pneumococcus 
causing  intense  diffuse  myeHtis  have  been  found  (Fig.  112). 

The  prognosis  is  very  grave,  but  not  absolutely  bad.  If  there  is 
reason  to  suspect  the  case  of  being  one  of  paralytic  rabies,  no  hope  can 
be  offered. 

Diagnosis.— This  must  be  made  from  the  ordinary  forms  of  acute 
poliomyelitis,  acute  myelitis,  acute  multiple  neuritis  and  periodic  family 
paralysis. 

Its  acute  ascending  course,  absence  of  fever,  of  anaesthesia,  of  atrophy, 
decubitus,  sphincter  troubles,  and  especially  the  absence  of  degenerative 
electrical  reactions,  of  a  family  history  with  a  history  of  previous  attacks 
are  sufficient  to  enable  one  to  make  the  diagnosis.  The  age  of  the 
patient,  and  the  presence  or  absence  of  an  alcoholic  history  should  be 
considered.  Lumbar  puncture  should  give  help.  (See  anterior  polio- 
myelitis.) 

Treatment. — This  consists  of  warm  baths  or  packs,  colon  washings, 
and  ehminative  treatment.  Large  doses  of  ergotin,  gr.  ij.,  every  hour 
have  been  successful  in  one  case.  Urotropin  should  be  given,  and  lumbar 
punctures  should  be  made. 


CHAPTER  XIII 


SCLEROSES,  DEGENERATIONS,  SYPHILIS 

Introductory. — The  term  sclerosis  is  somewhat  misleading.  Properly 
speaking,  it  is  the  fibroid  (and  neuroglia)  induration  which  results  from 
degeneration,  destruction  or  inflammatory  irritation.  We  speak  of 
degenerative  sclerosis,  of  an  inflammatory  and  of  a,  neuroglia  sclerosis,  or  of  a 
sclerosis  of  mixed  origin,  according  to  the  nature  of  the  primary  disease 
which  caused  it.  Some  writers  look  upon  primary  degenerations  as 
parenchymatous  inflammations.  There  is  no  objection  to  this  point  of 
view  as  long  as  we  agree  upon  the  essential  character  of  the  process. 
The  words  ''degeneration"  and  ''sclerosis"  are  often  used  to  indicate  the 
same  thing,  one  being  the  pathological  process,  the  other  the  anatomical 
result.  I  shall  use  the  term  "sclerosis"  here  in  its  pathological  sense, 
meaning  the  process  of  hardening,  in  presenting  a  classification  of  the 
degenerations  of  the  spinal  cord. 

I    Posterior  spinal  sclerosis  (locomotor 
I        ataxia). 
Lateral  sclerosis. 
Combined     sclerosis.       Hereditary 

ataxia. 
Progressive      muscular       atrophy, 
amyotrophic   lateral    sclerosis. 
/  Ascending  and  descending  degenera- 
\       tions. 

f   Chronic  myelitis  and  sclerosis  fol- 
Inflammatory,     infec-  I        lowing  destruction  of  cord.] 
tive.  [   Multiple  sclerosis. 


Spinal  scleroses. 


Primary  and  degenera- 
tive. Luetic,  toxic, 
connate. 

(Parenchymatous  in- 
flammation) 


Secondary, 
ical. 


physiolog- 


The  tendency  of  late  years  has  been  to  classify  diseases  of  the  nervous 
system  on  an  etiological  basis,  e.g.,  as  syphilogenous,  infectious,  tubercular 
but  I  believe  it  still  is  best  to  follow  the  clinical  and  anatomical  methods. 

Primary  degeneration  (parenchymatous  inflammation)  or  primary 
sclerosis,  as  one  may  say  for  convenience,  is  a  process  which  begins  in 
the  neuron  itself  and  ends  in  its  atrophy,  with  substitution  of  neuroglia 
and  connective  tissue.  As  to  its  nature,  so  far  as  the  microscope  shows 
us,  it  is  a  gradual  decay  and  death  of  the  neurons.  In  some  sclerotic 
processes,  like  locomotor  ataxia,  the  sclerosis  is  due  to  the  destruction 
of  the  neuron  by  the  toxic  activity  of  the  spirochceta  pallida.  The  decay 
is  accompanied  by  the  development  of  irritating  products,  leucomains 
toxalbumins,  which  may  produce  so  active  a  change  in  the  connective 

248 


SCLEROSES,    DEGENERATIONS,    SYPHILIS 


249 


tissue  as  to  lead  to  something  resembling  a  secondary  or  reactive  inflam- 
mation. This  is  never  of  high  grade,  however,  and  in  some  forms  of  tabes 
is  very  slight. 


Fig.   112. — Acute  ascending  myelitis  (^Landry's  paralj'sisj. 


Fig.  113. — Ascending  degeneration  in  third  cervical  segment,  from  transverse  lesion 
in  second  dorsal,  showing  degeneration  of  columns  of  Goll  and  cerebellar  tracts. 

In  progressive  muscular  atrophy  the  decay  and  death  produce  few 
irritating  products,  though  enough,  perhaps,  to  account  for  the  fibrillary 
twitchings  and  occasional  tremulous  condition  of  the  muscles. 


250 


DISEASES    OF    THE    NERVOUS    SYSTEM. 


The  ultimate  cause  of  these  degenerative  processes  is  the  micro-or- 
ganism of  syphilis,  toxins,  and  poisons,  and  congenital  defect  in  the  vitality 
of  the  neuron,  a  condition  called  by  Gowers  abiatrophy. 

Secondary  Degenerations  of  the  Spinal  Cord. — When  any  of  the  long- 
fibre  tracts  of  the  cord  are  cut  across  or  destroyed,  there  soon  results 
a  degeneration.  This  extends  up  or  down  in  accordance  with  the  direc- 
tion in  which  the  tracts  carry  impulses.  Thus,  when  the  crossed  py- 
ramidal tract  is  cut  across  the  degeneration  extends  down;  when  the 
column  of  GoU  is  involved  it  extends  up.  The  degenerative  process 
begins  almost  immediately  and  is  complete  in  a  few  weeks.  The  myelin 
sheath  swells,  gradually  breaks  up  and  disintegrates;  the  axis-cylinder  is 
involved  next.  At  the  same  time  the  connective  tissue  and  neuroglia 
proliferate  and  take  the  place  of  the  wasted  nerves.     Finally,  long  tracts 


Fig.  114. — Descending  degeneration  in  eighth  dorsal  segment  from  lesion  in  second 
dorsal,  showing  degeneration  in  direct  and  crossed  pyramidal  tract,  vestibulo-spinal 
and  comma  tracts. 

of  connective  tissue  have  taken  the  place  of  the  nerve  tissue.  The 
process  may  not  be  a  complete  one  if  the  lesion  does  not  entirely  destroy 
the  tract. 

Secondary  degenerations  complicate  and  add  to  the  pathological 
change  in  all  organic  diseases  of  the  cord.  In  brain  disease,  involving 
the  motor  tract,  as  in  hemiplegia,  secondary  degeneration  extends  into 
the  cord  and  adds  to  the  seriousness  of  the  disease.  Degenerations  of  the 
spinal  cord,  however,  do  not  extend  up  to  the  brain  to  any  extent,  except 
in  the  case  of  disease  of  the  antero-lateral  ascending  and  cerebellar 
tracts. 

Those  forms  of  sclerosis  found  in  chronic  myelitis  are  similar  to  the 
connective-tissue  scars  following  destructive  inflammation  elsewhere. 
A  person  who  has  a  chronic  myelitis  has  a  cicatrix  in  his  spinal  cord. 


SCLEROSES,   DEGENERATIONS,    SYPHILIS  251 

The  sclerosis  of  inultiple  sclerosis  is  probably  inflammatory  also,  but  it  is 
a  neuroglia  rather  than  a  connective-tissue  cicatrix. 

Short  Degenerating  Tracts. — ^By  the  use  of  more  delicate  stains  other 
degenerating  tracts  have  been  discovered.  These  are  described  under 
the  head  of  the  anatomy  of  the  spinal  cord. 

The  short-fibre  tracts  degenerate  only  a  little  way  up  and  down. 

SYPHILIS  OF  THE  NERVOUS  SYSTEM 

Syphilis  begins  to  attack  the  nervous  system  in  two  ways:  by  round- 
cell  infiltration  and  exudation  affecting  the  blood-vessels  of  the  meninges 
of  the  cord  and  brain;  and  by  the  development  of  a  parenchymatous 
degeneration  of  the  neurons. 
Hence  we  have: 

1 .  Meningo-vascular  or  exudative  syphilis  and 

2.  Parenchymatous  or  degenerative  syphilis. 

1.  Meningo-vascular  syphilis  takes  various  clinical  forms: 
(a)  Cerebral  syphilis. 

(6)   Spinal  syphilis. 

(c)   Cerebrospinal  syphilis. 

2.  Parenchymatous  syphilis  takes  the  forms  of: 
(a)  Paresis. 

(5)  Tabes  dorsalis. 

(c)  Muscular  atrophy. 

(d)  Combined  system  degeneration. 

(e)  Various  combinations  of  the  above. 

Epilepsy  and  optic  atrophy  are  added  by  Head  and  Fearnsides. 

In  many  cases  there  is  first  the  exudative  and  proliferative  syphilis, 
attacking  the  blood-vessels  and  meninges,  but  in  about  half  the  cases  this 
approach  is  so  slight  that  the  first  noticeable  effect  of  syphilis  of  the  nerv- 
ous system  is  a  degenerative  process.  Syphilis  begins  openly  to  attack  the 
nervous  system  in  from  two  to  twelve  years  after  infection,  but  it  may 
occur  within  six  months  or  as  late  as  thirty  years.  If  it  occurs  early  the 
meningo-vascular  form  dominates  and  may  be  the  only  one.  If  it  occurs 
late,  the  parenchymatous  and  degenerative  process  is  the  chief  and  often 
the  only  one. 

The  causes  leading  the  syphilis  organism  to  attack  the  nervous  system 
are  a  hereditary  weakness  or  predisposition;  abuse  of  the  nervous  system, 
especially  in  sexual  excesses  and  in  laborious  occupation  and,  finally,  the 
abuse  of  alcohol  and  food  and  the  adoption  of  a  mode  of  life  which  in  gen- 
eral tends  to  weaken  and  exhaust  the  system. 

There  is  some  evidence  that  mild  and  hardly  noticeable  forms  of  Syph- 
ilis are  those  most  likely  to  attack  the  nervous  centres  later.  It  is  a  fact 
that  in  about  half  the  cases  the  patients  deny  either  knowledge  of  any 
infection  or  of  the  development  of  secondary  cutaneous  symptoms  (rashes, 
sore  throat,  alopecia,  pains,  etc.).     This  apparent  immunity  of  the  cases 


252 


DISEASES    OF    THE    NERVOUS    SYSTEM 


with  flagrant  secondary  symptoms  may  be  due  in  part  to  the  fact  that 
these  latter  are  more  vigorously  treated.  The  absence  of  any  known  pri- 
mary lesion  is  explained  by  the  existence  of  an  infection  without  local 
reaction,  or  by  its  being  masked  by  a  gonorrhoea. 

Of  all  persons  affected  by  syphilis  it  is  probable  that  in  2  to  10 
per  cent,  the  nervous  system  becomes  involved.  Men  are  rather  more 
often  affected  than  women  with  nervous  syphilis,  and  rather  more  in  pro- 
portion to  the  infection  because  they  are  more  subject  to  the  exciting 
causes.  The  conditions  of  modern  civilization  have  increased  the 
amount  of  nervous  syphilis,  and  this  increase  is  mostly  in  the  degenerative 
types  of  paresis  and  tabes. 

Symptoms. — Since  syphilitic  changes  may  attack  any  part  of  the 
nervous  centres,  the  symptomatology  of  nerve  syphilis  is  necessarily  a 
varied  one.  The  reader  can  perhaps  best  understand  the  way  in  which 
the  disease  acts  by  having  presented,  first,  a  series  of  tables  showing  on 
the  one  side  the  clinical  symptoms,  on  the  other  the  chief  anatomical 
changes  that  underlie  them. 

I.  PRODROMAL  SYPHILIS. 
II.  MENINGO-VASCULAR  SYPHILIS 

(a)  Of  the  Brain. 

Clinical  Symptoms 

Severe  headache,  vomiting,  vertigo,  men- 
tal dullness,  and  irritability,  attacks  of 
somnolence  or  coma,  convulsions,  cra- 
nial-nerve palsies,  optic  neuritis,  hemi- 
plegia, brain  stem  and  bulbar  palsies, 
(fe)   Of  Brain  and  Cord. 

Many  of  the  brain  symptoms  as  above, 
spastic  paraplegia,  etc. 

(c)  Of  Spinal  Cord. 
Paraplegia,    Brown-S  e  q  u  a  r  d    paralysis. 

Muscular  atrophy.     Spastic  para- 
plegia and  ataxia. 

(d)  Of  the  Nerve-roots  and   Nerves. 
Cranial-nerve  palsies,  cauda-equina  symp- 
toms,    local    palsies    of    peripheral 
nerves.     Muscular  atrophy. 


(Hereditary  and  Acquired). 

Anatomical  Change 

Syphilitic  meningitis,  arteritis  and  phle- 
bitis. 


Meningitis;  diffuse,  disseminated,    or  lo- 
calized meningo-myelitis. 

Meningo-myelitis,  gumma,  localized  soft- 
enings   from    obliterative     arteritis. 


Root  neuritis,  gummatous  neuritis. 


III.  PARENCHYMATOUS  SYPHILIS 

(a)  Of  the  Brain. 
Paresis. 
Bulbar  palsy. 

(6)  Of  the  Cord. 
Tabes  dorsalis. 
Spastic  tabes. 
Muscular  atrophy. 

(c)    Of  Brain  and  Cord. 
Tabo-paresis. 

IV.  COMBINATIONS  OF  II  AND  III. 


(Hereditary  and  Acquired). 

Meningo-encephalitis. 


Meningo-myelitis . 


SCLEROSES,    DEGENERATIONS,    SYPHILIS  253 

I.  Prodromal  Syphilis. — The  development  of  syphilis  of  the  nervous 
system  is  often  preceded  by  prodromal  symptoms  of  a  definite  and 
recognized  character.  Such  symptoms  are  especially  apt  to  precede  paren- 
chymatous syphilis.     They  can  be  arranged  somewhat  as  follows : 

Meningeal  Prodromata.- — These  consist  of  annoying  and  often  severe 
headaches,  temporary  attacks  of  cranial  nerve  palsy;  attacks  of  dizziness; 
dyssesthesiae  which  are  particularly  referred  to  the  head  and  back  of 
the  neck.  They  are  symptoms  which  can  be  explained  by  the  supposition 
that  there  is  a  slight  grade  of  meningitis  in  some  part  of  the  brain  or 
cord  or  else  a  slight  degree  of  obliterative  arteritis  leading  to  local  or 
general  disturbances  of  the  brain  function. 

Luetic  Neurasthenia. — A  most  common  group  of  symptoms  is  one 
which  may  be  called  luetic  neurasthenia.  The  conditions  is  charac- 
terized by  some  mental  depression,  inability  to  use  the  brain  effectively 
or  long,  annoying  disturbances  in  the  shape  of  parsesthesia  of  the  head 
and  neck  and  extremities,  weakness  of  the  sexual  function,  and  the  general 
group  of  symptoms  which  come  under  the  description  of  neurasthenia  of 
a  rather  depressive  and  often  hypochondriacal  type. 

Luetic  Deterioration. — In  the  milder  forms  of  luetic  neurasthenia, 
there  is  not  so  much  an  absolutely  nervous  exhaustion  as  a  slight  change 
in  the  character  and  in  the  effectiveness  of  the  work  of  the  individual. 
For  a  number  of  years  before  the  development  of  a  frank  nervous  lues, 
for  example,  the  patient  will  have  been  recognized  as  having  become  a 
somewhat  different  person.  He  is  not  as  attentive  to  his  work  or  as  keen 
in  memory,  or  as  efficient  in  his  activities  generally.  He  is  more  irritable 
and  difficult  to  work  with  or  to  live  with. 

Luetic  Melancholia. — Parenchymatous  syphilis,  particularly  of  the 
paretic  or  tabo-paretic  type  is  not  infrequently  preceded  by  a  definite 
attack  of  melancholia  and  this  may  be  of  very  severe  hypochondriacal 
or  even  suicidal  character,  running  its  course  like  other  forms  of  melan- 
cholia. Much  less  frequently  the  infection  is  introduced  by  an  attack 
of  mania  which  may  be  mistaken  for  the  onset  of  true  paresis. 

II.  Meningo-vascular  S3^hilis. — Of  the  Brain. — In  its  most  common 
form  this  shows  itself  by  a  gradual  development  of  severe  and  persistent 
headache.  This  is  usually  associated  with  vertigo,  sometimes  with  nausea 
and  vomiting.  After  the  headache  has  developed  and  has  lasted  for  a  time, 
or  even  without  much  delay,  there  comes  on  sometimes  an  attack  of  hemi- 
plegia. Preceding  the  hemiplegia,  or  in  some  cases  without  the  hemiplegia, 
there  are  paralyses  of  the  cranial  nerves,  more  especially  of  the  nerves  of  the 
eye.  Optic  neuritis  is  somewhat  frequent.  The  pupils  may  be  irregular 
in  outline  and  sluggish  to  light.  There  may  be,  before  any  paralyses 
develop,  attacks  of  epileptic  convulsions,  either  general  or  partial. 
Without  any  paralyses  or  with  simply  cranial-nerve  paralyses,  there  may 


254  DISEASES    OF    THE    NERVOUS    SYSTEM 

develop  attacks  of  somnolence  and  coma.  Even  if  such  attacks  do  not 
appear,  the  patient  often  shows  a  mental  irritability  and  weakness,  a 
slowness  of  the  reasoning  process,  and  incapacity  to  fix  the  attention 
such  as  is  observed  in  connection  with  brain  tumors,  only  with  nerve 
syphilis  these  symptoms  are  not  usually  so  marked.  Polyuria  and  poly- 
dipsia are  symptoms  which  are  occasionally  met  with.  The  disease  may 
take  the  form  of  a  meningo-encephalitis  producing  symptoms  of  mental 
and  physical  disturbance  not  distinguishable  from  early  paresis  (men- 
ingo-vascular  paresis). 

Of  Brain  and  Cord. — Very  often  some  of  the  above  groups  of  symptoms 
are  associated  with  spinal  disease.  There  is  evidence  of  meningo- 
myelitis,  or  of  obliterating  arteritis  and  as  a  result,  we  have  paraplegia; 
or  the  meningeal  syphilis  of  the  brain  may  be  associated  with  degen- 
erative syphilis  and  we  have  lightning  pains,  ataxia  and  other  signs  of  an 
occurring  tabes. 

Of  the  Cord. — The  symptoms  in  spinal  syphilis  are  commonly  those  of 
a  transverse  myelitis  involving  most  often  the  lower  part  of  the  dorsal  and 
upper  part  of  the  lumbar  cord.  This  myelitis  usually  comes  on  rather 
slowly  with  the  ordinary  symptoms  of  a  chronic  or  subacute  transverse 
myelitis,  there  being  a  progressive  paraplegia  with  spasticity  of  the  legs 
and  a  good  deal  of  pain.  The  condition  is  known  as  syphilitic  spinal 
paralysis  (see  p.  230).  Spinal  syphilis  may  show  itself  also  by  the 
development  of  gummatous  nodules  which  grow  from  the  meninges,  press 
upon  the  cord,  and  produce  the  symptoms  of  a  spinal  tumor.  Spinal 
syphilis  more  rarely  develops  itself  in  three  or  four  different  foci,  produc- 
ing the  symptomatology  of  disseminated  myelitis.  Finally,  a  spinal 
endarteritis  may  lead  to  focal  hemorrhage  and  softening. 

Pathology. — I  have  already  given  some  indications  of  the  pathological 
changes  produced  by  syphilis.  The  disease  affects  the  nervous  system 
(1)  by  producing  a  meningitis  with  exudation,  (2)  by  producing  gum- 
matous masses,  (3)  by  producing  an  inflammation  of  the  arteries,  and 
(4)  by  so  influencing  the  neurons  so  as  to  lead  to  their  progressive  degen- 
eration. Of  all  these  forms  of  anatomical  change  it  is  the  arteries  that 
are  most  often  affected,  and  particularly  the  arteries  at  the  base  of  the 
brain. 

Syphilitic  meningitis  is  characterized  by  the  proliferation  of  round 
cells  and  the  preponderance  of  an  exudate  which  has  a  tendency  to  in- 
filtrate into  the  nervous  tissues.  The  anatomical  characteristics  of  the 
syphilitic  gumma  must  be  studied  in  special  text-books.  The  inflamma- 
tion of  the  arteries  attacks  first  the  external  coat  and  adventitia,  produc- 
ing there  an  enormous  multiplication  of  round  cells.  The  external  coat 
becomes  weakened,  and  as  a  result  there  develops  beneath  it,  between 
the  intima  and  the  elastic  layer,  another  exudate  which  constitutes  what 


SCLEROSES,    DEGENERATIONS,    SYPHILIS  255 

is  known  as  endarteritis.  In  syphilitic  arteritis,  therefore,  there  is  both 
a  peri-arteritis  and  an  endarteritis;  the  former  being  usually  the  primary 
and  most  essential  process.  The  endarteritis,  however,  as  it  develops 
gradually  produces  an  occlusion  of  the  arteries.  This  cuts  off  the  circu- 
lation of  the  blood  and  leads  to  softening  of  the  part.  There  is  also  a 
development  of  a  hyaline  degeneration  in  the  arteries,  which  some  regard 
as  a  very  essential  part  of  the  anatomical  change  (Fig.  116). 

Diagnosis. — -The  diagnosis  of  meningo-vascular  syphilis  is  based  upon 
the  history  of  an  infection,  the  irregularity  and  fugacity  of  the  symptoms, 
a  study  of  their  peculiar  clinical  characters  as  described  above.  But  all 
these  things  have  been  made  of  minor  importance  compared  with  those 
furnished  by  the  reactions  of  the  blood  and  the  character  of  the  cerebro- 
spinal fluid  (see- Serology  of  Syphilis). 

The  headache  of  syphilis  is  rather  characteristic.  It  may  attack  any 
part  of  the  head,  but  is  usually  unilateral  or  irregular,  or  again  it  may 
be  bilateral  in  its  distribution.  The  pain  is  very  intense  and  sometimes 
exhibits  a  certain  periodicity.  It  is  not  necessarily  worse  at  night.  It 
is  apt  to  last  continuously  for  from  five  days  to  three  or  four  weeks. 
Headache  of  this  character,  followed  by  the  paralysis  of  one  or  more 
cranial  nerves  or  by  an  attack  of  hemiplegia,  is  extremely  suggestive  of 
syphilis.  Optic  neuritis  is  very  liable  to  occur  when  the  disease  shows 
other  evidences  of  being  situated  at  the  base  of  the  brain.  This  optic 
neuritis  is  associated  with  contraction  of  the  visual  field,  and  a  charac- 
teristic feature  of  this  contraction  is  that  it  varies  a  great  deal  from  week 
to  week. 

Prognosis. — Unquestionably  the  outlook  is  much  more  favorable 
than  it  is  for  any  other  organic  disease  of  the  nervous  system.  When 
the  syphilitic  process  has  not  produced  so  much  arterial  disease  as  to 
lead  to  obliteration  of  vessels  and  softening,  a  very  great  degree  of  im- 
provement and  even  a  recovery  may  be  expected.  Headaches,  cranial 
and  other  nerve  palsies,  parsesthesias  and  the  neurasthenic  and  psychotic 
prodromata  of  exudative  syphilis  are  usually  curable.  Lesions  of 
the  convexity  are  usually  amenable  to  treatment.  Syphilitic  hemiplegia 
has  a  not  much  better  prognosis  than  hemiplegia  from  other  causes. 
Syphilitic  myelitis  has  a  not  very  good  prognosis,  but  it  is  better  than 
that  of  myelitis  due  to  trauma.  In  all  cases  the  results  are  enormously 
better  the  earlier  treatment  is  instituted.  Even  bulbar  and  spinal  paraly- 
ses, and  meningeal  or  exudative  paresis  are  curable  or  enormously 
relieved. 

Treatment. — A  laborious  life  full  of  worry  and  anxiety,  in  which  the 
patient  attempts  to  help  himself  along  with  stimulants,  is  surely  provoca- 
tive of  nervous  syphilis.     These  elements  of  cause  must  be  removed. 

In  recent  years  the  treatment  of  syphilis  by  hypodermic  injections 


256  DISEASES    OF    THE    NERVOUS    SYSTEM 

of  the  bichloride  or  saHcylate  of  mercury  has  been  widely  adopted,  and 
better  results  have  been  obtained  than  by  inunction  or  by  administra- 
tion by  the  mouth.  One  or  two  grains  of  the  salicylate  mixed  with  a 
liquid  petroleum  oil  may  be  given  twice  a  week.  The  effective  treatment 
of  nervous  syphilis  lies  at  present  in  the  wise  and  persistent  use  of  sal- 
varsan  combined  as  seems  needed  with  mercury  and  iodides,  tonics  and 
hygienic  measures.     The  details  are  given  under  Paresis. 

Other  drugs  which  are  of  value  are  the  ordinary  tonics,  such  as  iron, 
quinine,  and  the  bitters  and  mineral  acids.  Plenty  of  good  food,  out- 
door air,  and  all  those  things  which  will  improve  the  general  health  of 
the  patient  are  indicated. 

Syphilis  of  the  Nerves. — Syphilis  rarely  affects  the  peripheral  nerves; 
there  are,  however,  occasional  deposits  of  syphilitic  exudate  producing 
the  ordinary  symptoms  of  irritation  and  compression  of  nerves.  There 
is  said  to  be  a  form  of  multiple  neuritis  produced  by  syphilis,  but  its 
actual  existence  has  not  been  demonstrated.  Syphilis  is  sometimes  known 
to  attack  the  roots  of  the  cranial  nerves,  producing  a  root  neuritis. 
It  attacks  the  roots  of  the  spinal  nerves  when  the  spinal  membranes  are 
involved.  In  rare  cases,  where  it  involves  only  the  anterior  roots  it  causes 
a  form  of  muscular  atrophy. 

III.  Parenchymatous  Syphilis. — The  syphilitic  parenchymatous 
processes  lead  to  locomotor  ataxia,  general  paresis,  tabo-paresis,  pro- 
gressive spinal  paraplegia,  and  sometimes  to  a  form  of  muscular  atrophy 
due  to  parenchymatous  or  vascular  syphilis  of  the  anterior  horns. 

Meningeal  syphilis  may  be  combined  with  parenchymatous  forms,  so 
that  we  sometimes  see  locomotor  ataxia  associated  with  meningo-myelitis; 
and  we  see  paresis  associated  with  meningeal  syphilis. 

Hereditary  Syphilis. — ^Inherited  syphilis  will  lead  to  anatomical 
changes  and  clinical  manifestations  resembling  in  all  respects  those  of 
acquired  syphilis.  Inherited  syphilis,  in  other  words,  may  produce 
headaches,  cranial-nerve  palsies,  hemiplegia,  epilpsy,  mental  disorders 
juvenile  paresis,  feeble-mindedness,  and  degenerative  spinal  diseases. 
The  disease  probably  is  the  cause  of  a  considerable  proportion  of  the  cases 
of  chronic  hydrocephalus  and  of  many  of  the  cases  of  meningitis.  The 
peculiarities  of  hereditary  syphilis  show  themselves  rather  more  in  diffuse 
symptoms  such  as  would  be  attributed  to  a  meningitis  of  the  convexity  or 
circulatory  defects;  in  other  words,  convulsions  and  mental  weakness  are 
rather  more  frequent,  while  hemiplegia  and  cranial-nerve  palsies  are  com- 
paratively rare.  Hereditary  syphilis  also  rarely  attacks  the  spinal  cord, 
although  it  is  not  unlikely  that  it  is  a  factor  in  the  production  of  some  of 
the  hereditary  diseases  of  that  organ.  Hereditary  syphilis  develops  at 
any  time  from  birth  to  the  eighteenth  year,  but  most  commonly  under  the 
age  of  five  years.     Serological  tests  furnish  the  diagnosis. 


SCLEROSES,    DEGENERATIONS,    SYPHILIS  257 

The  presence  of  the  Hutchinson  teeth,  the  hazy  cornea,  and  deafness 
or  other  ear  trouble  were  the  old  diagnostic  criteria  of  hereditary  syphilis. 

LOCOMOTOR  ATAXIA 

{Posterior  Spinal  Sclerosis,  Tahes  Dorsalis) 

Definition. — Locomotor  ataxia  is  a  chronic  progressive  luetic  disease, 
involving  primarily  the  posterior  spinal  ganglia,  roots  and  neurons,  and 
later  the  spinal  cord  and  peripheral  nerves.  It  is  characterized  clinically 
by  inco-ordination,  pains,  anaesthesia,  and  various  visceral,  trophic  and 
other  symptoms,  and  anatomically  by  a  degenerative  sclerosis  chiefly 
marked  in  the  posterior  columns  of  the  cord  and  posterior  roots,  and  to 
a  less  extent  in  the  peripheral  nerves. 

Forms. — Besides  the  common  and  typical  form,  there  are  anomalous 
and  complicated  types. 


Types. 


1.  Common  form. 

2.  Neuralgic. 

3.  Paralytic. 

4.  With  initial  optic  atrophy. 


/-I        1-     X  J        f  With  muscular  atrophy. 
Complicated  „^.,,      ,.  ,  ^  -^ 

^  With  other  scleroses. 

With  general  paralysis. 


forms. 


Etiology.— The  disease  occurs  oftenest  in  middle  life,  between  thirty 
and  forty,  next  between  forty  and  fifty.  It  may  occur  as  early  as  the 
tenth  and  as  late  as  the  sixtieth  year.  In  the  very  early  cases  it  is  usually 
due  to  hereditary  syphilis.  It  is  much  more  common  in  males  (about 
10  to  1).  Hereditary  influence  is  only  indirect;  i.e.,  the  parents  may 
transmit  lues  or  a  neurotic  constitution.  Diathetic  influence  is  slight. 
Exposures  to  wet  and  cold,  combined  with  muscular  exertions,  are  effec- 
tive causes.  Soldiers,  travelers  and  drivers  are  rather  more  susceptible. 
Excessive  railroad  traveling,  excessive  dancing  with  exposure,  favor  the 
development  of  the  disease.  Excessive  sexual  intercourse,  combined 
with  irregular  living,  is  a  predisposing  cause. 

Syphihs  is  the  one  important  and  essential  cause.  A  personal  his- 
tory of  the  disease  is  obtained  in  from  60  per  cent,  to  90  per  cent,  of 
the  cases.  Serological  tests  show  almost  invariably  evidence  of  syphilis 
and  statistics  indicate  that  about  1  per  cent,  of  those  infected  with  syphilis 
become  tabetic  unless  treated  actively  and  by  modern  methods.^    Lack  of 

*  The  following  statistics  from  my  own  experience  show  the  physiognomy  of  the 
disease  in  a  cosmopolitan  American  city.  Total  cases,  248;  males,  226;  females,  22. 
Ages  when  disease  began:  Average  age  at  time  of  onset,  40;  beginning  a  year  or  two 
earlier  in  private  patients  and  in  those  with  a  history  of  syphilis  and  active  anti- 
syphilitic  treatment  (Collins).  Average  period  between  infection  and  tabes,  10  to  20, 
ranging  from  one  and  one-half  to  twenty-five  years.  This  is  much  longer  than  Erb's 
estimate,  but  is  reached  by  three  independent  studies  of  my  cases.     Average  duration 

17 


258  DISEASES    OF   THE    NERVOUS   SYSTEM 

proper  treatment  for  syphilis  is  believed  to  favor  the  development  of  the  dis- 
ease, but  a  careful  study  of  the  statistics  of  my  clinic  and  of  his  own  cases  by 
Dr.  Joseph  Collins  seems  to  show  that  antisyphilitic  treatment  as  formerly 
carried  out  does  not  prevent  the  disease  if  the  other  favoring  conditions, 
such  as  exhausting  work  and  sexual  or  alcoholic  excesses,  are  present. 

Among  exciting  causes  are  profoundly  depressing  emotions,  acute  infec- 
tive diseases  like  typhus,  pneumonia  and  rheumatism,  difficult  labors  with 
severe  hemorrhage,  prolonged  lactation  and  excessive  smoking.  Edinger 
lays  great  stress  on  the  over-use  of  the  limbs.  Trauma  as  an  apparently, 
exciting  cause  is  noted  in  a  very  small  percentage  of  cases  (less  than  1  per 
cent.).  In  my  experience  there  has  always  been  evidence  that  the  disease 
was  already  in  the  system  but  had  not  been  recognized  in  these  cases. 

Symptoms. — ^The  disease  is  generally  divided  into  three  stages:  the 
initial  or  pre-ataxic,  the  ataxic  and  the  paralytic. 

1 .  The  pre-ataxic  or  initial  stage.  Previous  to  any  other  notable  symp- 
toms, the  patient  may  have  for  months  or  years  attacks  of  sharp  pains  dart- 
ing through  his  limbs  or  about  his  trunk.  With  this  he  may  have  only 
Argyll-Robertson  pupils  and  loss  of  knee-jerks  and  ankle-jerks  or  of  ankle- 
jerks  alone.  To  this  may  be  added  a  little  uncertainty  of  gait.  Or 
instead  of  the  pains  he  may  have  for  a  long  time  gastric  crises.  Occasionally 
nothing  is  noted  at  first  but  loss  of  sexual  power  or  a  weak  bladder. 

A  gradual  development  of  optic  atrophy  and  blindness  may  also  pre- 
cede nearly  all  other  symptoms.  Ocular  palsies  and  hypotonia  may  also 
be  among  the  preataxic  symptoms.  In  many  cases  the  disease  does^not 
advance  beyond  the  preataxic  stage,  and  this  is  particularly  true  of 
neuralgic  and  optic  forms  of  tabes. 

When  the  ataxic  process  sets  in,  in  addition  to  the  symptoms  men- 
tioned the  patient  notices  a  slight  uncertainty  in  walking,  especially  at 
night;  he  has  numb  feelings  in  his  feet.  His  sexual  function  becomes 
weak,  his  control  over  the  bladder  slightly  impaired.  He  has  temporary 
attacks  of  vertigo  and  of  double  vision.  A  sense  of  weariness  oppresses 
him,  even  though  he  has  made  no  exertion.  He  may  have  attacks  of 
vomiting  and  gastralgia,  and  may  suffer  from  constipation,  with  hemor- 
rhoids and  rectal  pains.  Arthropathies  may  appear.  Some  hypotonia 
may  be  present.  Such  symptoms  may  last  a  few  months  or  several  years ; 
often  the  disease  is  kept  in  this  stage. 

2.  The  ataxic  stage.     The  gait  now  becomes  so  unsteady  that  others 

of  disease  when  seen  by  me,  eight  years;  average  duration  of  Ufe  in  five  fatal  cases, 
twelve  years,  ranging  from  five  to  twenty  years.  Comphcations:  optic  atrophy, 
6  per  cent. ;  marked  arthropathies,  5  per  cent. ;  with  general  paresis,  4  per  cent. ;  para- 
plegia, 1.5  per  cent.;  hemiplegia,  1.6  per  cent.;  eye  palsies,  8  per  cent.  About  10  per 
cent,  of  300  private  cases  were  complicated  with  paresis — tabo-paresis.  The  compli- 
cation is  smaller  in  dispensary  cases.  High  tabes  (arm  tabes),  5  per  cent.;  cranial 
nerve  palsies,  10  per  cent.;  ophthalmoplegia  in  1  case,  progressive  muscular  atrophy 
in  3,  laryngeal  palsies  in  3. 


SCLEROSES,    DEGENERATIONS,    SYPHILIS  259 

notice  it;  the  patient  has  to  have  help,  and  when  walking  he  has  to  watch 
his  feet  and  the  ground.  If  he  stands  with  his  eyes  closed,  he  totters  and 
may  fall.  His  feet  feel  as  though  there  was  a  layer  of  cloth  or  cotton 
between  the  soles  and  the  ground.  Paroxysms  of  lightning-like  pains 
continue  to  attack  the  legs,  chest  and  arms;  tests  show  anaesthesia  of  the 
toes  and  feet  or  in  areas  on  the  legs  and  on  the  trunk.  A  sense  of  con- 
striction is  felt  around  the  waist.  The  sexual  power  is  lost;  the  bladder 
is  weak,  and  care  has  to  be  taken  to  empty  it.  The  bowels  are  consti- 
pated; at  times  he  has  attacks  of  intense  pain  in  the  epigastrium,  with 
vomiting  and  perhaps  a  diarrhoea  coming  on  without  cause.     The  pupils 


"i-^jt 


Fig.  115. — Meningo-vascular  disease  in  syphilis  of  brain  and  cord.     {Bruce.) 

are  small  often  unequal  and  irregular  and  do  not  react  to  light,  but  do 
react  to  accommodation;  vision  is  still  good.  The  incoordination  and 
pain  and  anaesthesia  after  a  time  affect  slightly  the  arms.  The  muscles 
become  relaxed  and  atonic.  The  face  shows  atonia;  also  there  is  often 
a  pseudo-ptosis  of  one  or  both  lids.     This  stage  lasts  several  years. 

3.  The  paralytic  stage.  After  several  years  with  various  remissions 
and  improvements,  the  patient  loses  altogether  the  power  of  walking. 
His  legs  are  somewhat  wasted,  but  the  muscular  strength  is  fairly  good. 
The  anaesthesia  and  ataxia  are  very  great.  The  patient  does  not  feel  the 
prick  of  a  pin  or  touch  of  the  hand;  nor  with  closed  eyes  does  he  know 
where  his  legs  are.  His  bladder  is  anaesthetic  and  paretic,  so  that  the 
urine  has  to  be  drawn.  The  pains  are  much  less,  but  are  still  present  at 
times.     The  arms  are  more  involved,  but  never  so  seriously  as  to  make 


260 


DISEASES    OF    THE    NERVOUS    SYSTEM 


them  useless  like  the  legs.  The  intelligence  remains  good,  and  the  patient 
may  continue  bedridden  for  years,  dying  finally  from  some  intercurrent 
affection. 

The  following  table  shows  the  prominent  symptoms  in  the  usual  order 
of  their  appearance :  ^ 


First  stage 
(half  to  thirty  years) 

Second    stage 
(two  to  ten  years) 

Third  stage 
(two  to  ten  years) 

Motor 

[  Eye  palsies. 

Ataxia. 

i 

Muscular  weakness  and 
hypotonia. 

Less. 

Increased. 
Paresis,  increased. 
Increased. 

Increased. 

Paraplegia. 
Increased. 

Sensory 

1  Pains. 

1   

Pains.                             Painless. 

Anaesthesia.                   Increased. 

1 

Excito-reflex 

Loss  of  knee-jerk. 
A.-R.  pupil. 

Trophic 

Arthropathies. 

More  rare. 

Rare. 

Visceral 

Sexual  weakness. 
Vesical  weakness. 
■   Constipation. 

Gastric  crises. 

Increased. 

J 

Decreased. 

Increased. 
Decreased. 

Special  senses 

j  Diplopia. 

■   Optic  atrophy. 

Rare. 
Rare. 

Deafness. 

Increased. 
Increased. 

Analysis  of  Symptoms. — A  study  of  the  symptoms  in  tabes  produces 
enormous  results  in  the  way  of  clinical  phenomena.  The  student  should  not, 
however,  lose  his  sense  of  proportion  in  going  over  these  data.  After  all,  the 
serious  things  in  tabes  are  not  so  numerous.  They  are  his  ataxia  and  loss 
of  ability  to  walk  well,  his  pains,  sexual  and  bladder  weakness,  hypotonia, 
anaesthesia,  crises,  especially  gastric,  arthropathies,  and  optic  atrophy. 

Locomotor  and  static  ataxia  are  present  very  early,  but  only  to  a 
moderate  extent.  Tests,  such  as  making  the  patient  walk  and  stand 
with  the  eyes  closed,  noting  the  position  of  limbs  and  the  weight  of 
objects,  will  reveal  an  ataxia  due  largely  to  beginning  anaesthesia  of  the 
joints  and  tendons. 

^  The  disease  attacks  different  levels  of  the  cord  in  about  the  following  proportion : 
Optic  tabes,  5  per  cent. ;  high  (arm)  tabes,  5  per  cent. ;  dorsal  (abdominal  and  trunk) 
tabes,  20  per  cent. ;  lumbar  and  sacral  tabes,  60  per  cent.  To  these  add  tabo-paresis, 
10  per  cent. 


SCLEROSES,    DEGENERATIONS,    SYPHILIS 


261 


The  patella-tendon  reflex  or  knee-jerk  is  abolished  very  early  in  all 
typical  cases.  This  constitutes  a  very  important  symptom,  therefore. 
The  ankle-tendon  reflex  is  lost  early  in  the  disease,  but  not,  as  a  rule,  so 
early  as  the  patella  reflex.  Inequality  or  diminution  in  the  activity  of 
these  reflexes  are  significant  when  taken  in  connection  with  other  symp- 
toms. An  inequality  is  more  im- 
portant than  a  general  diminu- 
tion. These  reflexes  of  knee  and 
ankle  may  disappear  early  in  the 
disease  and  return  under  treat- 
ment, but  this  is  rare  and  later 
they  may  disappear  again. 

The  gait  and  station  in  ataxia 
are  characteristic.  In  walking, 
the  patient  keeps  his  eyes  on  the 
ground  and  on  his  feet.  The  lat- 
ter he  throws  out  rather  forcibly, 
owing  to  over-action  of  the  exten- 
sors of  the  foot.  In  watching 
such  a  patient  walk  barefooted, 
the  extensor  tendons  can  be  seen 
to  stand  out  with  each  forward 
movement  of  the  limb.  The  foot 
is  brought  down  sharply  on  the 
heel  and  the  legs  are  spread  apart 
a  little.  Turning  a  corner,  turn- 
ing around  and  going  downstairs 
are  done  awkwardly,  and  the  pa- 
tient is  apt  to  totter  and  fall. 
Walking  on  a  chalked  line  is  very 
difficult;  so  also  is  walking  back- 
ward. The  gait  improves  after 
the  patient  walks  a  while,  and  he 
will  generally  say  that  the  prac- 
tice of  walking  does  him  good. 
Still,  he  soon  gets  tired  (Fig.  116). 

Hypotonia,  or  relaxation  and  lengthening  of  the  tendons  and  muscles, 
is  usually  an  early  and  always  an  important  symptom,  but  is  sometimes 
not  very  marked  until  later  in  the  disease.  This  is  what  causes  the  genu 
incurvatum;  when  present  in  high  degree  it  is  an  unfavorable  sign,  for  it 
is  apt  to  lead  to  deformities  and  promote  arthropathies  (Figs.  118,  122). 

Myoclonic  and  tic-Hke  spasms  may  affect  the  face  and  body. 

Myokymia  (fibrillary  and  wave-like  contractions  of  the  muscles)   is 


Fig.  116. 


-Showing  station  in  second  sta| 
of  locomotor  ataxia. 


262 


DISEASES    OF   THE    NERVOUS   SYSTEM 


an  early  and  rare  complication.  It  occurs  usually  in  cases  with  rather 
rapid  onset,  and  affects  most  the  muscles  of  the  lower  limbs.  Though 
not  painful,  it  is  a  very  annoying  phenomenon. 

Severe  rectal  neuralgia,  associated  perhaps  with  hemorrhoids,  is 
sometimes  an  early  symptom.  Persistent  neuralgia  and  functional  dis- 
turbance of  the  bladder  and  rectum  should  cause  suspicion  of  ataxia. 
Lancinating  or  lightning  pains  occur  and  are  very  characteristic.  The 
pains  dart  down  the  legs  along  the  course  of  the  sciatic,  or  they  suddenly 
appear  as  patches  of  pain  on  the  foot  or  leg  or  thigh  ("spot  pains  ")•  The 
pain  comes  unexpectedly  and  with  such  severity  that  the  patient  involun- 
tarily jumps  or  jerks  the  hmb.  He  speaks  of  his  "jerking"  and  ''twitch- 
ing pains."  The  pains  may  affect 
the  bowels  or  be  felt  as  a  squeez- 
ing sensation  around  the  waist 
(girdle  pains).  The  pains  of  ataxia 
are  often  the  most  obstinate  and 
distressing  symptom.  They  usu- 
ally come  on  in  great  intensity  once 
or  twice  a  month,  and  last  for  two 
or  three  days.  They  then  leave  the 
patient  for  a  time.  They  are  often 
worse  in  cold  and  damp  weather. 
In  some  cases  the  pains  are  almost 
continuous,  coming  on,  if  not  every 
day,  at  least  two  or  three  times  a 
week.  Such  cases  are  associated 
with  much  cutaneous  hyperses- 
thesia,  especially  during  the  attacks.  This  type  of  cases  is  called  "the 
neuralgic."  The  patients  rarely  have  as  much  ataxia,  paresis  or  visceral 
troubles  as  the  typical  forms  present,  and  in  certain  respects  such  cases 
are  favorable.  Sometimes  the  pains  are  accompanied  with  erythema 
or  herpes  zoster  showing  an  acute  involvement  of  a  posterior  ganglion. 
The  pains  of  the  disease  continue  well  into  the  second  and  even  third 
stage.  Meanwhile  the  anaesthesia  becomes  much  more  marked.  It  af- 
fects most  the  feet  and  next  the  legs,  rarely  extending  much  over  the  thighs, 
but  passing  to  the  fingers  and  hands.  The  anaesthesia  is  greatest  to  pain, 
but  touch  and  temperature  sense  are  also  involved.  There  is  often  de- 
layed conduction  and  polyaesthesia;  and  many  other  curious  perversions  of 
the  cutaneous  sense  are  noted.  Some  anaesthesia  usually  develops  over 
the  finger  tips  and  hands,  and  sometimes  a  band  of  anaesthesia  devel- 
ops about  the  trunk  (Fig.  119).  This  trunk  anaesthesia  may  be  one  of 
the  early  symptoms  of  the  disease.  The  facial  and  cranial  nerves  are  not 
much  affected,  but  there  may  be  trigeminal  neuralgia.     The  olfactory 


Fig.  117. — Hypotonia  in  late  tabes  dorsalis. 


SCLEROSES,    DEGENERATIONS,    SYPHILIS 


263 


nerve  is  occasionally  affected.  In  early  stages  of  the  disease  when  there  is 
perhaps  some  specific  disorder  of  the  mucous  membrane,  parosmia  occurs, 
the  patient  being  annoyed  with  the  sense  of  a  bad  smell.  Later  in  tabes 
this  sense  may  be  lost. 

Optic  atrophy  occurs  in  about  6  per  cent,  of  cases  in  my  experience. 
Optic  atrophy  usually  develops  in  the  preataxic  stage,  and  if  a  patient  has 
reached  the  second  stage  without  it,  he  will  probably  escape  it  altogether. 
Cases  with  ocular  paralyses  are  slightly  more  disposed  to  it  (Berger).  It 
attacks  the  left  eye  oftener  than  the  right.  The  atrophy  begins  sometimes 
with  increased  sensibihty  to  hght,  flashes  of  hght,  and  muscai  volitantes. 


Fig.  118. — Hypotonia  in  locomotor  ataxia. 


With  the  failing  vision,  disturbance  of  color  sense  often  and  contraction 
of  the  visual  field  always  occur.  This  contraction  is  irregular,  with 
sector-formed  defects;  not  hemiopic.  The  atrophy  progresses  slowly 
with  slight  remissions.  It  may  cease  its  progress,  but  this  is  rare  and 
blindness  comes  in  about  three  years.  Ophthalmoscopically,  there  may 
be  seen  slight  evidence  of  congestion  in  the  early  stage ;  later,  pallor  of  the 
discs,  which  finally  become  grayish. 

The  eye  muscles  are  implicated  in  some  way  in  nearly  all  cases  of 
tabes.  The  fohowing  are  the  disorders:  (1)  Loss  of  the  hght  reflex  and 
myosis;  (2)  sympathetic-nerve  ptosis;  (3)  paralysis  of  the  external  eye 
muscles. 


264 


DISEASES    OF   THE    NERVOUS   SYSTEM 


Paralyses  of  the  ocular  muscles  (third,  fourth  and  sixth)  occur  rather 
oftener  in  cases  with  evidence  of  exudative  (meningeal)  syphilis. 
Ocular  palsies  are  early  symptoms  of  the  disease,  occurring,  as  a  rule, 
in  the  preataxic  stage. 

1.  Loss  of  light  reflex  and  pupillary  rigidity.  The  pupils  are  small 
and  sometimes  uneven  and  irregular  in  shape;  they  respond  to  accom- 
modation, but  not  to  light.  In  early  stages  the  light  reflex  may  be 
simply  sluggish.     In  the  late  stages  the  pupils  are  often  dilated.     The 


Fig.  119. — Trunk  and  leg  anaesthesia  in  early  stage  of  tabes  dorsalis. 


phenomenon  is  perhaps  due  to  lesion  of  the  ciliary  ganglia.  More 
probably  it  is  due  to  degeneration  of  the  mesial  nucleus  of  the  third 
nerve,  or  its  connections.  The  Argyll-Robertson  pupil  is  practically 
found  only  in  tabes  and  in  general  paresis.  It  may  be  brought  about 
by  local  disease,  by  a  polioencephalitic  or  ganglionic  infection,  or  it  may 
be  congenital.  The  ocular  skin  reflex  usually  disappears  early.  The 
myosis  in  tabes  is  due  to  paralysis  of  the  sympathetic  dilating  fibres. 

2.  Sympathetic  nerve  ptosis.  A  slight  drooping  of  one  or  both  lids 
is  not  infrequent.  It  begins  early  and  progresses  slightly  up  to  the  later 
stages  of  the  disease.     It  is  due  to  paralysis  of  the  cervical  sympathetic- 


SCLEROSES,    DEGENERATIONS,    SYPHILIS  265 

nerve  fibres  which  go  to  the  unstriatecl  fibres  of  the  levator  palpebrae 
(tarsalis  superior). 

3.  Paralysis  of  the  external  eye  muscles.  The  external  rectus  is 
oftenest  affected  of  single  muscles,  but  the  various  branches  of  the  third 
nerve  taken  together  are  oftener  involved  than  the  sixth.  Of  the  third 
nerve's  branches,  the  levator  palpebrae  and  internal  recti  muscles  are 
oftenest  involved.  There  may  be  multiple  palsies.  These  occur  oftener 
with  meningeal  syphilis.  Progressive  ophthalmoplegia  may  be  associ- 
ated with  tabes.  The  ocular  nerve  palsies  may  be  transitory  or  perma- 
nent. Those  occurring  in  the  preataxic  stage  are  usually  transitory, 
lasting  a  few  hours,  days  or  weeks.  Cases  have  even  lasted  two  years 
and  got  well.  The  permanent  palsies  develop  usually  in  the  later  stages. 
The  early  palsies  are  usually  due  to  a  syphilitic  exudation  at  the  base  of 
the  brain;  the  late  palsies  are  usually  due  to  degenerative  lesions  of  the 
nuclei  of  the  ocular  nerves. 

Violent  neuralgic  pains  sometimes  occur  in  the  face,  but  it  is  rare; 
in  fact,  a  characteristic  of  tabetic  pains  is  that  they  hardly  ever  involve 
the  trigeminus.  However,  it  does  occur  that  a  typical  tic  douloureux 
may  develop. 

Paralysis  of  the  seventh  nerve,  though  not  infrequent  in  cerebral 
syphilis,  is  not  a  symptom  in  tabes.  It  is  not  even  a  premonitory 
symptom  as  are  the  ocular  palsies.  Spasmodic  movements  of  the  lips 
and  face  with  smacking  movements  similar  to  those  seen  in  some  forms 
of  spasmodic  tic  have  been  noted  in  two  of  my  patients. 

The  acoustic  nerve  is  frequently  affected,  some  form  or  degree  of  deaf- 
ness occurring  in  about  one-fourth  of  the  cases;  but  in  the  majority  of 
instances  the  trouble  is  an  accidental  complication  due  to  middle-ear 
disease.  Primary  atrophy  of  the  auditory  nerve  is  very  rare,  as  might 
be  expected,  since  this  nerve  is  structurally  not  like  the  optic  nerve.  Its 
existence  has  been  inferred  on  clinical  grounds.  There  is  a  form  of  tabetic 
deafness  of  trophic  origin  due  to  a  sclerotic  condition  of  the  middle  ear 
(Treitel).  The  labyrinthine  nerve  is  affected  but  rarely.  Vertigo  is  not 
common,  yet  labyrinthine  crises  causing  seizures  like  those  of  Meniere's 
disease  have  been  observed. 

Dyscesthesia  of  the  throat  with  attacks  of  repeated  swallowing  move- 
ments form  what  Oppenheim  calls  pharyngeal  crises. 

Bulbar  jparalysis  as  well  as  progressive  muscular  atrophy  are  rare 
association  diseases  and  generally  appear  late  in  the  course. 

More  common  are  disorders  of  innervation  of  the  larynx.  These  con- 
sist of  laryngeal  crises  and  paralyses  of  the  laryngeal  muscles.  The 
characteristic  paralysis  of  tabes  is  a  ''posticus  palsy;"  i.e.,  a  paralysis 
of  the  posterior  crico-thyroid  muscles.  These  are  abductors,  and  their 
paralysis  causes  difficulty  in  breathing  if  both  are  affected  and  sometimes 


266  DISEASES    OF   THE    NERVOUS   SYSTEM 

when  one  is  affected.  The  paralysis  is  usually  unilateral.  The  laryngeal 
palsies  are  usually  early  symptoms  and  usually  are  not  serious.  I  have 
known,  however,  sudden  death  to  occur  in  a  patient  subject  to  attacks 
of  this  type  of  palsy.     Anaesthesia  of  the  throat  and  larynx  is  very  rare. 

In  a  laryngeal  crisis  there  is  spasm  of  the  adductors  or  paralysis  of 
abductors,  with  noisy,  croupy  respiration.  The  attacks  come  on  sud- 
denly, the  patient  coughs  and  struggles  for  breath,  and  he  may  be  seized 
with  vertigo  and  fall  down.  The  pulse  may  be  very  fast.  The  paroxysm 
lasts  for  a  few  minutes  to  several  hours.  The  symptoms  are  very 
distressing,  but  not  usually  dangerous. 

Paroxysms  of  cough  have  been  described  as  "bronchial  crises." 

There  are  also  cardiac  crises,  in  which  there  are  dyspnoea  and  rapid 
heart  beat  and  sense  of  suffocation  resembling  angina.  A  much  more 
frequent  symptom  is  a  rapid  pulse  which  runs  about  one  hundred  and  is 
small  and  weak. 

The  heart  is  sometimes  diseased,  either  from  neurotrophic  disturb- 
ance or  luetic  degeneration.  The  pulse  is  often  small,  rather  rapid, 
and  weak. 

The  most  common  and  distressing  of  the  crises  of  tabes  are  the  gastric. 
These  sometimes  occur  in  the  preataxic  stage  and  recur  for  a  long  time 
before  the  nature  of  the  trouble  is  recognized.  They  consist  of  sudden 
attacks  of  intense  pain  extending  from  the  groin  to  the  epigastrium  or 
encircling  the  waist,  accompanied  by  vomiting  and  sometimes  diarrhoea. 
The  attacks  are  often  associated  with  pains  in  the  legs.  They  last  two 
or  three  days,  then  usually  pass  away,  but  some  cases  last  two  or  three 
weeks  and  leave  the  patient  much  exhausted  and  often  more  ataxic. 
Sometimes  instead  of  or  between  the  crises  the  patient  has  a  continual 
diffuse,  dull,  abdominal  pain. 

The  arthropathies  of-  locomotor  ataxia.  Degenerative  diseases  of  the 
joints,  technically  known  as  arthropathies,  and  spontaneous  fractures 
of  bones  form  important  symptoms  of  tabes.  They  occur  in  10  per  cent. 
(Charcot)  or  5  per  cent,  (author)  of  cases. 

The  arthropathies  are  three  or  four  times  more  frequent  than  the 
fractures.  The  joints  oftenest  affected  are  the  knees,  ankles  and  hips; 
but  the  elbow,  shoulder,  wrist,  vertebral  and  pelvic  bones  and  small 
joints  may  be  attacked. 

Spontaneous  fractures  occur  oftenest  in  the  shaft  and  neck  of  the 
femur,  next  in  the  legs,  forearm,  humerus,  and  clavicle.  The  pelvis, 
scapula,  vertebrae  and  under  jaw  may  be  fractured.  Arthropathies  are 
often  accompanied  by  fractures,  especially  of  the  heads  of  the  bones. 
The  two  sides  of  the  body  are  about  equally  affected. 

The  arthropathies  are  characterized  by  a  sudden,  apparently  spon- 
taneous painless  swelling  of  the  joint.     The  symptoms  may  develop  in 


SCLEROSES,    DEGENERATIONS,    SYPHILIS 


267 


twenty-four  or  forty-eight  hours.  In  rare  cases  there  is  a  history  of 
some  preceding  rheumatic  pains  or  of  an  injury.  After  a  time  there  is  an 
osseous  hyperplasia  of  the  joint,  which  becomes  enlarged  to  enormous 
proportions.  There  is  also  a  tendency  to  luxation  of  the  joint.  It  crepi- 
tates on  moving.  There  is  no  tenderness  on  pressure;  the  hand  finds 
evidence  of  synovial  exudation,  roughened  surfaces,  and  perhaps  frac- 
tures of  the  enlarged  parts.  In  the  milder  forms  there  are  simply  swell- 
ing from  synovial  exudation  and  some  enlargement  of  the  bones  with 
roughened  surfaces.  After  a  few  weeks  this  swelling  may  subside  and 
the  joint  return  to  nearly  its  nat- 
ural size.  In  other  cases  the 
process  progresses,  the  ligaments 
relax,  the  bones  of  the  joint  can  be 
moved  about  freely,  and  luxations 
are  easily  produced.  There  is 
still  no  pain,  but  the  limb  becomes 
almost  or  entirely  useless  on  ac- 
count of  the  loose  and  relaxed 
condition  of  the  parts  (Fig.  121). 
As  time  goes  on,  some  absorption 
takes  place  and  the  head  of  the 
bone  may  almost  disappear.  The 
arthropathies  have  been  divided 
into  benign  and  malignant,  but  no 
sharp  line  can  be  drawn  or  cer- 
tain prognosis  made  in  the  early 
stage.  The  arthropathies  appear 
in  the  prodromal  and  early  stage 
of  the  disease  in  over  half  the 
cases,  and  are  often  at  first  unrec- 
ognized. One-third  occur  after 
the  tenth  year  of  the  disease. 

The  spontaneous  fractures  are 
usually  brought  on  by  a  slight  trauma,  such  as  a  fall.  Violent  muscular 
movements  may  produce  them.  They  also  are  painless,  as  a  rule.  The 
fractures  usually  heal  well,  often  with  abnormal  readiness,  but  occasion- 
ally there  is  delay,  and  often  healing  is  accompanied  by  great  throwing 
out  of  callus. 

Pathologically,  the  arthropathy  is  a  rarefying  osteitis.  It  does  not 
differ  anatomically  from  arthritis  deformans,  except  that  fractures  may 
accompany  it.  Clinically,  the  chief  difference  lies  in  the  abruptness, 
spontaneity  and  painlessness  of  the  process.  The  disease,  on  the  whole, 
cannot  be   considered   specifically   different  from   arthritis   deformans, 


Fig.  120. — Arthropathy  of  shoulder. 


268 


DISEASES    OF    THE    NERVOUS    SYSTEM 


modified  by  the  analgesia  of  the  parts.  It  is  due  probably  to  a  degenera- 
tive change  in  the  nerves  supplying  the  joints  and  bones.  The  process 
may  begin  in  the  cartilage,  bone  or  ligaments.  Eventually  all  these 
parts  are  involved.  There  is  congestion  of  the  synovial  membranes  with 
hydrarthrosis,  then  atrophy  and  rarefying  hypertrophy  of  the  epiphyses, 
relaxation  of  the  ligaments,  formation  of  osteophytes  and  bony  stalac- 


FiG.  121. — Arthropathy  of  knees. 

tites.     There  may  be  a  rarefying  osteitis  of  the  long  bones,  without  much 
joint  involvement  at  first. 

Various  trophic  disturbances  of  the  skin  may  appear,  generally  late  in 
the  disease.  The  most  common  are  herpes  and  lichen.  Besides  these, 
bullae,  transitory  erythema,  urticaria,  eczema,  pemphigus,  ecthyma, 
ulcers,  ichthyosis  and  petechias  have  been  described;  but  they  are  rare 


SCLEROSES,    DEGENERATIONS,    SYPHILIS 


269 


and  often  only  accidental  complications.  A  peculiar  round  perforating 
ulcer  sometimes  develops  on  the  sole  of  the  foot,  often  as  the  result  of 
cutting  a  corn.  In  rare  cases  the  nails  and  teeth  fall  out.  In  frankly 
syphilitic  cases  there  is  usually  baldness.  The  skin  of  the  tabetic  patient 
loses  its  "tone"  due  probably  to  the  general  muscular  atony  and  to  weak- 
ness of  the  erectores  pilarum.  At  any  rate,  the  hand  has  a  character- 
istic flabby  feeling  which  is  almost  diagnostic  of  the  disease.  The  face 
and  cutaneous  tissue  generally  show  the  same  characteristic. 

A  sense  of  great  weariness  and  heaviness  in  the  limbs,  present  con- 
stantly, no  matter  how  much  rest  is  taken,  is  a  characteristic  early 
symptom,  and  is  due  to  an  irritability  of  the  nerves  of  muscular  sensibility. 

Muscular  atrophies  occur  sometimes  in 
tabes.  They  are  of  three  kinds:  (1)  a  pro- 
gressive muscular  atrophy  due  to  local  end- 
arteritis and  resulting  degeneration  of  trophic 
and  motor  cells  (chronic  poliomyelitis);  (2) 
localized  muscular  atrophies  due  to  degenera- 
tive atrophy  of  nerves;  (3)  a  general  wast- 
ing. Under  the  first  head  one  finds  ophthal- 
moplegia, bulbar  paralysis  and  spinal  myop- 
athies; under  the  second,  wasting  of  certain 
groups  of  muscles  in  the  legs  or  arms. 

Besides  these,  there  is  a  generalized  atro- 
phy which  occurs  in  the  paralytic  stage  and 
is  due  probably  to  a  slight  involvement  of 
the  anterior  horns  in  the  progressive  process 
that  affects  the  cord. 

Attacks  of  hemiplegia  in  rare  instances 
occur  in  tabes.  They  are  usually  of  tempo- 
rary character  and  occur  early  in  the  disease. 
They  may  come  on  late  and  are  then  more 

likely  due  to  acute  softening  due  to  disease  of  the  cerebral  vessels  of 
syphilitic  origin. 

Acute  paraplegia  comes  on  occasionally  also,  and  this  sometimes 
almost  disappears. 

The  sexual  power  may  be  at  first  greatly  exaggerated;  but  this  is  rare, 
and  usually  there  is  progressive  weakness  and  loss  of  desire.  The  bladder 
and  sexual  functions  are  rarely  entirely  lost  and  rarely  equally  impaired  in 
the  first  stage;  one  may  continue  good  while  the  other  is  affected  moder- 
ately.    Usually  the  sexual  function  goes  first. 

Some  cerebral  symptoms  occur  in  tabes,  chiefly  in  the  early  stage. 
They  are  insomnia,  which  may  be  very  obstinate,  and  occasional  vertigo. 
An  irritability  of  temper  and  tendency  to  despondency,  sometimes  noted, 


Fig. 


122. — Perforating 
of  foot. 


ulcer 


270  DISEASES    OF   THE    NEEVOUS   SYSTEM 

cannot  be  considered  unnatural.  Apoplectiform  and  epileptiform  attacks 
are  described,  but  are  very  rare,  and  should  cause  a  suspicion  of  a  com- 
plication. The  disease  in  very  rare  cases  terminates  in  general  paresis. 
Usually  if  there  is  to  be  paresis  it  comes  on  with  the  tabes.  When  the 
disease  developes  frankly  and  typically  as  locomotor  ataxia,  paresis  rarely 
supervenes. 

Course,— The  disease  has  been  termed  progressive,  but  it  is  not  so  in 
a  large  number  of  cases.  With  proper  treatment  the  symptoms  can  often 
be  kept  in  control  for  years.  The  first  stage  may  last  twenty  years  or 
more;  the  second  stage  five  to  fifteen  years.  The  total  duration  of  the 
disease  varies  enormously,  ranging  between  three  and  thirty  years.  A 
few  acute  cases  have  been  observed,  running  a  course  of  less  than  a  year. 

Complications. — These  are  acute  myelitis,  generally  syphilitic;  lateral 
sclerosis,  progressive  muscular  atrophy,  hemiplegia  from  embolism  or 
endarteritis,  general  paresis  and  heart  disease. 

Tabo -paresis. — In  a  rather  increasing  number  of  cases  one  sees  the 
symptoms  of  paresis  and  tabes  develop  together.  In  these  cases  the 
cerebral  symptoms  are  usually  more  dominant  and  are  always  more  seri- 
ous and  important.  These  symptoms  do  not  differ  greatly  from  the  ordi- 
nary early  symptoms  of  paresis.  The  tabetic  symptoms  are  often  of  less 
note  and  consist  in  loss  of  knee-jerks,  some  ataxia,  lancinating  pains, 
ocular  palsies  and  vesical  and  sexual  weakness.  Taking  a  group  of  100 
cases  of  tabes  I  find  about  10  per  cent,  are  tabo-paretic.  In  these 
cases  it  is  the  paresis  that  has  to  be  more  carefully  watched  and  dealt 
with.     Like  tabes,  it  can  be  arrested,  but  not  so  often  as  in  the  pure  type. 

Pathological  Anatomy  and  Pathology. — The  characteristic  changes  in 
an  advanced  case  are  found  in  the  spinal  cord,  posterior  spinal  ganglia 
and  posterior  roots,  and  to  a  less  extent  in  the  peripheral  nerves.  The 
spinal  cord  usually  is  reduced  in  size  and  flattened  antero-posteriorly; 
the  pia  mater  is  thickened  somewhat.  One  can  see  with  the  naked 
eye  that  the  posterior  columns  of  the  cord  are  shrunken  and  have  a 
grayish  appearance. 

In  early  cases  one  sees  that  the  part  of  the  posterior  column  first 
affected  is  a  vertical  streak  lying  in  the  middle  root  zone  between  the 
posterior  median  (columns  of  GoU)  and  posterior  external  columns 
(columns  of  Burdach)  (Fig.  123).  The  segments  first  and  most  affected 
are  those  of  the  upper  lumbar  and  lower  dorsal  region.  Besides  this  area 
the  rim  zone  or  column  of  Lissauer  is  also  early  involved.  As  the  disease 
progresses  it  extends  upward  and  spreads  laterally  so  that  finally  all  of 
the  posterior  column  is  changed  into  a  dense  connective-tissue  mass 
through  which  only  a  few  nerve-fibres  run.  The  part  last  and  least 
involved  is  that  lying  just  posterior  to  the  commissure  (anterior  root 
zone  of  Flechsig,  ventral  fundamental  column)    and    that    lying  just 


SCLEROSES,    DEGENERATIONS,    SYPHILIS 


271 


Fig.  123.  Fig.  124. 

Fig.  12.3. — ^Locomotor  ataxia,  showing  areas  affected  in  first  stage  at  five  different 
levels.  Drawn  from  specimens  in  author's  possession  and  from  comparative  study  of 
over  thirty  other  figures. 

Fig.  124. — ^Locomotor  ataxia,  second  stage. 


272  DISEASES    OF   THE    NERVOUS    SYSTEM 

mesial  of  the  posterior  horns  (external  part  of  the  middle  root  zone) 
(Fig.  125).  There  is  sometimes  a  degeneration  of  the  antero-lateral 
ascending  tract  (Gowers'  tract),  and  very  rarely  of  the  cerebellar  tract. 
The  pyramidal  tracts  are  involved  only  in  complicated  cases.  The  cells 
and  fibres  of  the  column  of  Clark  are  often  involved  in  advanced  cases. 
The  gray  matter  of  both  the  posterior  and  anterior  horns  may  show  some 
degenerative  changes,  viz.,  decrease  of  the  fibre  network  and  atrophy  of 
the  cellular  elements. 

The  posterior  roots  are  usually  involved,  the  process  extending  as  far 
as  the  spinal  ganglia,  which  also  show  some  degeneration,  but  the  lesion 
is  not  strikingly  marked  here  in  all  cases,  and  sometimes  the  spinal  ganglia 
are  nearly  healthy,  although  the  posterior  columns  are  diseased.  The 
anterior  roots  are  fairly  normal. 

The  exact  initial  point  of  attack  varies,  and  this  accounts  for  the  va- 
riation in  the  symptoms.  Cases  that  begin  with  decided  bladder  and  geni- 
tal symptoms  probably  start  low  down;  cases  which  go  for  a  good  while 
with  only  ataxia,  loss  of  knee-jerk,  and  pains  begin  higher;  while  in  the 
brachial  or  arm-type  cases  the  process  begins  in  the  cervical  enlargement. 

The  peripheral  nerves  are  diseased  in  a  large  number  of  the  ad- 
vanced cases.  The  nerves  of  the  leg  are  most  involved.  The  process 
is  a  degenerative  atrophy  or  neuritis.  It  affects  the  extremities  of 
the  nerves  first  and  slowly  extends  upward,  seldom  reaching  the  large 
trunks. 

Sometimes  the  disease  begins  in  the  optic  nerves,  but  not  in  the  bipo- 
lar visual  cells  of  the  retina  which  correspond  to  the  posterior  ganglion 
cells.  The  process  here  is  an  atrophy  beginning  at  the  periphery  and 
extending  brainward.  The  third,  fifth  and  sixth  nerves  are  occasionally 
involved;  still  more  rarely  the  olfactory  and'  auditory.  The  vagus 
nerve  and  sometimes  its  nucleus  and  that  of  the  glossopharyngeal  are 
implicated,  it  may  be,  rather  early  in  the  disease.  It  is  believed  that  these 
facts  explain  many  of  the  laryngeal  and  visceral  crises  and  the  tachycardia. 

Pathology. — Syphilis  often  invades  the  nerve-centres  before  true  tabes 
sets  in  and  frankly  shows  itself  in  the  form  of  inflammatory,  meningeal, 
vascular  and  gummatous  exudates,  but  often  it  does  not  betray  its 
presence  in  this  way  but  does  its  fatal  work  quietly  through  years  of 
apparent  health.  All  the  time  its  poison  is  at  work  instituting  a  tendency 
to  death  and  degeneration  in  certain  parts  of  the  nerve-centres.  The 
parts  which  are  usually  first  selected  are  the  posterior  spinal  roots  and 
the  neuraxons  which  pass  from  the  nerve-cells  of  the  ganglia  into  the 
posterior  roots  and  columns  of  the  spinal  cord.  Locomotor  ataxia,  there- 
fore, is  not  primarily  a  disease  of  the  posterior  spinal  columns,  but  of 
the  peripheral  sensory  neurons.  It  is  true  that  the  posterior  spinal 
ganglia  are  not  always  so  seriously  diseased  as  the  posterior  columns  of 


SCLEROSES,    DEGENERATIONS,    SYPHILIS 


273 


the  cord.  This,  however,  is  because  the  severity  of  the  disease  is  first 
shown  in  the  central  neuraxons  of  the  gangha  and  their  collaterals,  just 
as  in  alcohoHc  neuritis  the  peripheral  parts  of  the  motor  neuraxons 
are  most  and  earhest  affected  by  alcohol.  The  spirochceta  toxin  is 
carried  in  the  peri-radicular  spaces  and  starts  often  a  radiculitis  or  root 


Fig.  125. — Tabes  dorsalis,  advanced  stage;  cervical  dorsal  and  lumbar  levels. 


degeneration,  which  extends  into  the  cord.  As  the  disease  extends,  it 
involves  both  the  peripheral  and  central  parts  of  these  sensory  neurons; 
that  is  to  say,  both  the  sensory  fibres  and  the  posterior  spinal  roots. 
Still  later  it  attacks  other  portions  of  the  nerve-centres.  The  syphilitic 
microbe  and  its  toxins  are  brought  to  the  nerve-centres  in  the  blood, 

18 


274  DISEASES    OF    THE    NERVOUS    SYSTEM 

whence  may  pass  into  the  lymphatic  sheaths  of  the  blood-vessels  or 
are  thrown  out  upon  the  serous  membranes  in  the  subdural  sacs.  In 
the  circulation  of  the  cerebrospinal  fluid  the  toxins  are  carried  along  the 
serous  sheaths  which  surround  the  cerebrospinal  nerve-roots.  The 
nerves,  as  they  pass  out  from  the  spinal  cord,  are  covered  with  three 
membranes;  the  dura  mater,  the  arachnoid  and  the  pia  mater.  The 
dura  and  the  arachnoid  surround  them  less  tightly  than  the  other. 
The  dura  becomes  fused  with  the  connective  tissue  supporting  the  nerves 
as  they  pass  out,  and  the  arachnoid  becomes  fused  with  the  epineurium 
and  perineurium.  Now,  fluid  injected  into  either  the  subdural  or  sub- 
arachnoid spaces  passes  readily  along  the  nerves  for  some  distance  (Mace- 
wen),  and  syphilitic  toxins  in  the  subarachnoid  and  subdural  spaces  of  the 
spinal  cord  will  thus  have  a  tendency  to  infiltrate  along  these  sheaths,  but 
as  it  passes  out  of  the  vertebral  canal  or  cranial  cavity  it  meets  mechan- 
ical obstacles,  owing  to  the  constriction  of  the  parts,  and  there  is  therefore 
a  certain  damming  up  or  accumulation  of  the  poisonous  material  at  these 
points  of  exit.  Generally  at  this  point  it  meets  with  the  posterior  spinal 
ganglion  a  highly  organized  structure  with  special  vascular  supply,  and 
it  therefore  naturally  deposits  its  poison  upon  this  part,  which  furnishes 
much  more  opportunity  for  mischief  than  the  non-vascular  anterior  roots. 
It  is  a  fact  that  many  of  the  initial  symptoms  of  locomotor  ataxia  are 
thus  connected  with  such  troubles  as  would  occur  from  an  exudate  trying 
to  get  out  along  the  course  of  the  spinal  or  cranial  nerves.  A  frequent 
initial  symptom,  for  example,  is  palsy  of  one  of  the  third  nerves  or  of  the 
sixth  or  seventh  nerves,  due  to  exudates  clinging  around  their  roots.  Still 
more  frequently  the  initial  symptom  is  a  neuralgic  pain  in  the  course  of 
the  sciatic  plexus,  due  to  the  effects  of  this  poison  upon  the  ganglia.  It 
has  been  established  that  the  syphilitic  infection  is  due  to  the  spirochceta 
pallida.  These  organisms  have  been  found  in  tertiary  forms  of  syphilis, 
and  it  has  been  shown  that  the  spirochceta  is  alive  and  acting  upon  the 
nervous  system,  even  in  degenerative  or  parasyphilitic  stage.  Thus  the 
degenerations  of  tabes  are  really  only  a  later  form  of  a  constantly  acting- 
infection  and  all  the  phenomena,  both  of  syphilis  proper  and  so-called 
parasyphilis  are  only  different  stages  of  the  same  pathological  process. 

I  assume  in  this  description  that  it  is  a  syphilitic  poison  which  is  al- 
ways at  work  as  a  cause  of  tabes  dorsalis.  This,  however,  may  not  neces- 
sarily be  the  case,  for  it  may  be  the  infection  of  other  diseases;  and  the 
results  of  other  poisons,  such  as  ergot,  pellagra,  etc.,  may  be  explained 
in  the  same  way.  There  is  an  inadequacy  of  the  lymphatic  and  venous 
systems  thoroughly  to  rid  the  spinal  canal  of  the  poisons  that  lie  in  it ; 
the  body  of  the  cord  is  cleared,  but  the  roots  do  not  get  rid  of  the 
poison. 

As  to  why  this  process  attacks  some  persons  and  not  others,  it  can  only 


SCLEROSES,    DEGENERATIONS,    SYPHILIS  2/0 

be  said  that  certain  people  are  born  with  defective  power  of  resistance 
as  regards  their  nerve-centres,  and  that  others  induce  this  defective 
state  by  physical  and  other  excesses. 

Diagnosis. — In  the  first  stage  the  disease  has  to  be  distinguished  from 
hereditary  ataxia,  multiple  neuritis,  chronic  myelitis,  spinal  tumor,  spinal 
syphilis,  general  paresis  and  neurasthenia.  In  hereditary  ataxia  the  age, 
the  history  of  the  disease,  and  the  absence  of  lightning  pains  are  usually 
sufficient  to  distinguish  it.  Multiple  neuritis,  in  its  sensory  or  pseudo- 
tabetic  form,  sometimes  resembles  closely  locomotor  ataxia.  The  differ- 
ential points  are  given  in  the  sections  devoted  to  that  disease.  In 
myelitis  there  is  more  paralysis,  generally  exaggeration  of  reflexes,  and 
an  absence  of  disturbance  of  special  senses. 

The  serological  formula  in  tabes  varies,  but  it  is  about  as  follows : 

Ser.  Wassermann  —  or  -f- 

Cer.  spinal  fluid  Wassermann  +  or  — 

Globulin  -f- 

Cells  30  to  50 

This  formula  is  changed  to  negative  by  active  and  thorough  treat- 
ment. It  becomes  negative  in  very  advanced  periods  of  the  disease. 
(See  Paresis.) 

The  diagnostic  criteria  of  locomotor  ataxia  in  all  cases  are  the  pres- 
ence of  lightning  pains,  numbness  of  the  feet,  loss  of  knee-jerk,  hypotonia, 
arthropathies,  ataxia  of  station  and  gait,  without  much  loss  of  muscular 
power,  the  presence  of  the  Argyll-Robertson  pupil,  the  history  of  syphilis 
and  the  slow  onset  of  the  disease.  These  criteiia  apply  especially  for 
the  early  stages  of  the  progressing  disease.  A  lost  knee-jerk,  lightning 
pains,  a  positive  serological  formula  and  stiff  pupils  are  usually  quite 
enough  to  assure  a  diagnosis. 

Prognosis. — -In  the  first  stage  a  large  percentage  may  have  the  disease 
stopped  and  get  practically  well;  and  tabes  dorsalis,  if  seen  early  and  prop- 
erly treated,  is  no  longer  a  progressive  disease.  In  the  second  stage  a  cure 
is  impossible,  but  great  improvement  may  be  secured  and  the  patient 
made  relatively  comfortable  for  years. 

In  the  third  stage  little  can  be  done  except  to  relieve  the  symptoms, 
but  life  may  be  prolonged.  In  some  cases  the  careful  application  of 
mechanical  therapy  (the  Frenkel  exercises)  will  enable  patients  to  walk  to 
some  extent  again.  The  malady  is  of  course  better  controlled  if  the 
patient  can  afford  to  lead  a  regular  and  quiet  life.  This  is  one  of  the 
diseases  in  which  the  poor  man  has  not  as  good  a  chance,  because  hos- 
pitals will  not  keep  him  long  enough. 

Death  usually  occurs  from  some  intercurrent  malady  or  from  kidney 


276  DISEASES    OF    THE    NERVOUS    SYSTEM 

disease  caused  by  the  bladder  trouble.  Patients  very  rarely  indeed  die 
from  the  disease  itself  and  its  various  ''crises." 

Treatment. — ^The  treatment  of  locomotor  ataxia  is  a  subject  the 
discussion  of  which  cannot  be  made  dogmatic,  for  the  treatment  depends 
very  largely  upon  the  patient  and  the  stage  and  type  of  the  disease. 
My  experience  is  that  any  treatment  depends  enormously  upon  one's 
opportunities  of  getting  the  patient  in  the  earliest  stages.  Supposing 
this  be  done,  the  first  thing  is  to  be  quite  assured  that  there  is  no  trace  of 
syphilis  in  the  system  as  shown  by  clinical  signs  and  by  tests  of  the  blood 
and  cerebrospinal  fluid. 

It  is  the  fashion  now  to  begin  treatment  by  giving  intra-venous  or 
intra-spinous  injections  of  salvarsan.  Brilliant  results  have  been  secured 
and  perhaps  better  or  more  uniform  results  than  from  the  use  of  mercury 
and  iodide.  Injections  of  neo-salvarsan  0.9  may  be  given  twice  weekly 
until  ten  doses  have  been  given.  In  the  intervening  days  inunctions  or 
hypodermics  of  mercury  should  be  given  in  average  doses.  After  this, 
hypodermics  of  salicylate  of  mercury,  gr.  i.  may  be  given  twice  a  week  for 
six  weeks.  Then  the  patient  should  be  given  tonics  and  general  hygienic 
measures.  If  at  the  end  of  two  months,  the  serological  formula  is  not 
markedly  improved  another  course  of  injections  is  given.  If  the  patient 
is  much  better  or  if  the  formula  has  become  negative,  the  salvarsan  need 
not  be  given  oftener  than  twice  a  year. 

The  serological  formula  may  become  normal  under  ordinary  hygienic 
conditions  especially  if  the  patient  lives  in  the  open  air.  This  is  a  clinical 
fact  which  should  be  borne  in  mind.  If  the  disease  is  accompanied  by 
evidences  of  meningeal  (exudative)  syphilis,  the  treatments  may  need  to 
be  doubled  in  intensity. 

It  is  sometimes  stated  that  the  iodides  are  not  needed,  or  do  no  good 
in  tabes,  but  this  is  not  the  case.  After  salvarsan  and  mercurial  treat- 
ment patients  sometimes  improve  further  under  the  iodide  of  sodium  in 
moderate  or  large  doses.  Indeed  forty  years  ago  nearly  as  much  was 
claimed  by  good  observers  for  massive  doses  of  iodide  as  is  now  claimed 
for  salvarsan. 

Along  with  these  first  medicinal  measures,  the  physician  should  pre- 
scribe something  which  is  also  most  important,  and  that  is  simply  rest. 
Every  patient  with  locomotor  ataxia  should  at  once  have  the  importance 
of  rest  strongly  impressed  upon  him,  and  the  prescription  of  sixteen  weeks 
a  large  part  of  the  time  in  bed  is  sometimes  advisable.  Equally  good 
results  can  be  usually  obtained,  however,  by  obliging  the  patient  to  go 
through  a  simple  and  regular  life,  involving  moderate  walking  and  no 
hard  physical  work.  Institutional  life  for  three  months  is  of  enormous 
advantage.  It  is  a  rule  to  which  I  have  seen  hardly  an  exception  that 
tabetic  patients  brought  to  the  hospital  improve  in  a  striking  way  simply 


SCLEROSES,    DEGENERATIONS,    SYPHILIS  277 

from  the  quiet  routine  of  life  there,  and  despite  the  thinness  of  city  milk 
and  the  uncertain  value  of  hospital  eggs. 

The  drugs  which  are  used  as  tonics  are  mainly  the  nitrate  of  strychnia, 
iron,  the  preparations  of  arsenic  and  phosphorus.  The  various  prepara- 
tions of  the  phosphates,  such  as  glycero-phosphate  of  lime,  the  hypophos- 
phite  of  lime,  phosphoric  acid,  seem  to  be  of  some  benefit.  Strychnine 
occasionally  does  good  in  small  doses,  but  unless  very  carefully  increased 
large  doses  may  lead  to  disastrous  results  and  it  should  always  be  given 
with  caution.  A  great  many  other  drugs  may  be  given  for  the  relief  of 
symptoms.  Thus  ergot,  belladonna,  and  urotropin  sometimes  help  the 
bladder.  The  fluid  extract  of  buchu  in  doses  of  twenty  drops,  combined 
with  ten  drops  of  the  tincture  of  hyoscyamus,  is  also  useful.  For  the 
pain,  phenacetin  is  a  drug  which  gives  satisfaction.  It  may  be  com- 
bined with  bicarbonate  of  sodium,  with  codein;  or  some  of  the  other 
coal-tar  products,  such  as  antipyrin,  antifebrin,  pyramidon,  maj'-  be 
substituted.  A  teaspoonful  of  baking  soda  internally  will  sometimes 
stop  the  pains.  Small  doses  of  strychnine  may  be  combined  with 
this.  Small  amounts  of  strychnine  can  always  be  given  for  the  sexual 
weakness,  but  the  dose  should  rarely  be  made  a  large  one.  For  the 
gastric  crises,  nothing  is  so  good  as  a  hypodermatic  injection  of  mor- 
phine, and  for  the  severe  crises  of  pain  an  occasional  hypodermic  of 
morphine  should  be  given.  The  locomotor  ataxic,  however,  who  becomes 
addicted  to  the  use  of  morphine  for  his  pains  is  indeed  in  a  hopeless  con- 
dition. In  persistent  constipation  the  diet  should  be  light  and  mainly 
of  vegetables  and  of  liquids,  such  as  milk,  broths,  etc.  In  persistent 
diarrhceal  states  I  have  found  ichthyol  of  use.  This  drug  also  relieves 
the  pains. 

The  annoying  insomnia  is  to  be  treated  by  fresh  air,  lukewarm  baths 
and  sea-shore  life.  If  drugs  must  be  used,  bromide  of  lithium  with  a 
few  grains  of  chloral,  paraldehyde  in  not  over  thirty-drop  doses  or  the 
veronal  group  are  the  best. 

In  neuralgia  of  the  rectum  and  bladder,  suppositories  containing  iodo- 
form and  belladonna,  or  codein,  or  antipyrin,  may  be  used.  Sometimes 
simple  gelatin  or  gluten  suppositories  act  very  well.  Some  of  the  cases 
of  rectal  neuralgia  or  hypersesthesia  are  due  to  insufficient  clearing  of  the 
lower  bowel  when  a  movement  occurs,  and  if  the  patient  washes  out  the 
bowel  with  a  pint  of  warm  water  after  each  movement  he  is  very  much 
more  comfortable. 

There  is  no  diet  which  has  a  specific  effect  upon  locomotor  ataxia, 
but  the  patient  should  be  given  those  foods  which  are  non-fermentative 
and  digestible. 

Hydrotherapy  is  of  considerable  benefit.  The  most  efficient  of  the 
single  measures  is  the  lukewarm  bath  at  a  temperature  of  about  95°F. 


278  DISEASES    OF    THE    NERVOUS    SYSTEM 

for  ten  or  twenty  minutes  daily.  After  the  bath  it  is  well  to  have  a 
little  cold  water  poured  over  the  back  and  then  the  patient  should  be 
diligently  rubbed.  In  most  cases  a  simple  lukewarm  bath  is  quite  as 
effective  as  anything.  In  others  the  patient  feels  better  if  there  is  added 
to  it  some  slight  stimulant  to  the  skin,  e.g.,  two  tablespoonfuls  of  pine- 
needle  extract;  or  a  regular  pine-needle  bath  or  Nauheim  bath  may  be 
given.  The  Charcot  douche  given  in  moderate  strength  is  helpful  in 
cases  that  are  not  advanced  or  particularly  weak.  I  have  some  hesita- 
tion in  recommending  any  special  watering-places  or  cures.  I  have  had 
patients  return  benefited  from  the  Hot  Springs  of  Virginia  and  other 
American  resorts.  In  Europe,  the  baths  at  Lamalou,  France,  and  at 
Nauheim,  Germany,  have  some  reputation.  Hot  baths  are  sometimes 
injurious,  and  bathing  may  be  overdone  by  the  ataxic. 

Electricity  is  of  use  from  its  general  tonic  and  reflex  effects,  and  it 
perhaps  exercises  some  direct  influence  on  the  diseased  process.  Strong 
galvanic  currents  (15  to  30  ma.)  should  be  applied  along  the  spine,  through 
the  trunk,  and  down  the  legs  and  arms.  The  combined  galvanic  and 
faradic  current  is  even  better,  given  in  the  same  way.  The  faradic  brush 
may  be  applied  over  the  anaesthetic  extremities  and  along  the  back. 

The  actual  cautery  is  occasionally  efficient  in  stopping  pains.  It 
should  be  applied  to  the  back  as  often  as  twice  a  month  at  least  and  some- 
times twice  a  week.  Large  dry  cups  may  be  applied  rapidly  and  in  great 
number  (80  to  100)  along  the  spine  and  along  the  course  of  the  sciatic 
nerves.  They  make  the  patient  feel  better  and  relieve  sometimes  the 
sense  of  exhaustion.  In  very  painful  cases  occasional  wet  cups  and  leeches 
are  useful. 

I  still  find  that  suspension  by  the  neck  and  arms  is  helpful  in  some 
cases.  It  is  best  adapted  to  persons  in  the  second  stage  and  to  those 
who  have  a  good  deal  of  bladder  trouble  and  pain.  It  is  of  little  value 
in  the  paralytic  stage,  and  must  be  used  with  care  in  the  early  stage  and 
when  patients  are  large  and  heavy.  Suspensions  should  be  given  for 
from  one  to  three  minutes  three  times  a  week  until  twenty-five  or  thirty 
are  taken.     After  three  months  a  second  course  may  be  given. 

The  treatment  of  locomotor  ataxia  by  systematic  exercises,  known 
as  the  Frenkel  method,  is  one  that  has  been  effectively  used.  It  con- 
sists in  having  the  patient  go  through  regular  exercises  which  teach 
him  to  co-ordinate  the  different  groups  of  muscles  of  the  trunk,  legs  and 
arms.  The  Frenkel  method  is  one  which  can  be  given  with  advantage 
to  persons  who  are  passing  into  the  second  stage  of  tabes  and  in  whom 
the  disease  is  not  making  progress.  It  is  especially  indicated  where 
there  is  not  great  hypotonia.  It  must  be  used  very  carefully  and  for  a 
long  time.  It  often  enables  the  patient  to  walk  better  and  use  his  arms 
better,  but  it  does  not  especially  affect  the  progress  of  the  disease. 


SCLEROSES,   DEGENERATIONS,    SYPHILIS 


279 


Finally,  it  has  seemed  to  me  that  those  sufferers  from  locomotor 
ataxia  do  best  who  persistently  and  courageously  fight  against  their 
malady.  Those  who,  despite  suffering  and  discomfort,  will  three  or  four 
times  a  year  take  medicinal  treatment,  and  some  hydro-therapeutic  or 
electric  measures  such  as  will  have  beneficial  effect  upon  their  general 
nutrition  and  such  as  will  buoy  up  their  hopes  and  improve  their  mental 
condition,  are  quite  sure  to  be  rewarded.  After  a  hard  fight  they  will 
emerge  into  a  state  of  comparative  relief  from  their  symptoms  and 
secure  a  measurable  degree  of  rest  from  the  progress  of  their  disease. 

LATERAL  SCLEROSIS 

{Spastic  Sjyinal  Paralysis) 

Adult  Form. — Spastic  spinal  paralysis  or  spastic  paraplegia  is  a 
malady  due  to  disease  of  the  lateral  columns  and  especially  the  pyramidal 


Fig.  126. — ^Lateral  scleroses  witti  spastic  paraplegia  showing  degeneration  of 

pyramidal  tracts. 

tracts  of  the  spinal  cord.  As  these  tracts  are  diseased  and  injured  in 
many  ways  and  by  many  causes,  spastic  spinal  paralysis  is  a  very  com- 
mon condition.  It  is  symptomatic  of  transverse  myeUtis,  of  multiple 
sclerosis  and  of  tumors  and  other  pathological  conditions  which  cause 
pressure  on  the  cord.     It  occurs  in  the  cerebral  diplegias. 

There  is,  however,  one  condition  in  which  in  adults  the  lateral  columns 
and  especially  the  pyramidal  tracts  undergo  primary  degeneration,  and 
thus  we  speak  of  primary  lateral  sclerosis,  causing  a  form  of  spastic 
paraplegia  which  is  an  individual  disease  (Fig.  126).  It  is  a  very  rare 
condition;  its  existence  was  long  doubted,  but  it  has  now  been  established. 


280  DISEASES    OF   THE    NERVOUS   SYSTEM 

It  is  a  chronic  malady  characterized  by  progressive  spasticity  and  weak- 
ness of  the  legs  and  later  of  the  arms,  by  increase  of  the  reflexes,  the  de- 
velopment of  contractures  and  by  the  absence  of  sensory  disturbances 
and  sphincter  troubles.  The  disease  develops  between  the  ages  of 
twenty  and  forty.  The  causes  are  unknown,  except  that  there  is  one 
type  of  the  disease  which  is  of  hereditary  origin.  Syphilis,  acute  infec- 
tions and  toxic  substances  are  sometimes  associated  with  its  develop- 
ment. Poisoning  by  certain  kinds  of  lathyrus  cause  symptoms  of  the 
disease. 

In  the  hereditary  or  familial  form  the  disease  affects  different  mem- 
bers of  many  succeeding  generations  in  the  family.  In  the  cases  so  far 
described  it  begins  early  in  life,  affects  only  or  mainly  the  legs  and  runs  a 
very  slow  course  unaccompanied  by  pain,  ataxia  or  visceral  symptoms. 
Both  the  acquired  and  the  familial  forms  may  last  for  twenty  or  thirty 
years. 

The  special  symptoms  of  the  disease  are  the  same  as  those  which  occur 
in  involvement  of  the  pyramidal  tracts  from  other  causes,  and  are  described 
under  the  head  of  myelitis. 

In  the  diagnosis  of  the  disease  one  has  to  exclude  pathologically  the 
spinal  form  of  multiple  sclerosis,  chronic  transverse  myelitis,  compression 
paraplegia  from  vertebral  disease  and  from  tumors.  The  disease  is  so 
rare  that  particular  pains  must  be  taken  to  rule  out  these  more  common 
disorders. 

The  Congenital  Form  (Little's  Disease).- — Etiology  .—The  term 
spastic  spinal  paralysis,  is  also  applied  to  an  affection  which  is  al- 
ways of  congenital  or  infantile  origin  and  is  due,  it  is  supposed,  to 
a  lack  of  development  of  the  pyramidal  tracts.  This  lack  of  develop- 
ment leads  to  a  sclerosis  of  the  lateral  columns  of  the  spinal  cord  and 
to  symptoms  of  rigidity  of  the  legs  and  arms,  exaggeration  of  the  re- 
flexes, with  some  real  muscular  weakness  and  atrophy.  The  disease  is 
of  prenatal,  natal  or  infantile  origin,  being  due  to  some  developmental 
defect  or,  as  Little  supposed,  to  premature  and  forced  deliveries,  with 
probably  some  meningeal  hemorrhage  on  the  convexity  of  the  brain. 
Through  these  causes  the  pyramidal  tracts  cease  to  grow,  or,  at  least, 
this  process  is  greatly  delayed.  In  many  cases  there  is  a  premature  birth 
and  difficult  labor. 

Symptoms. — The  malady  is  noticed  within  a  short  time  after  birth, 
usually  within  a  year,  but  it  may  be  delayed  in  family  types  to  the  fifth 
year  or  even  later.  Some  cases  of  Little's  disease  may,  it  is  believed, 
develop  as  late  as  after  maturity.  It  is  not  my  purpose  to  give  a  descrip- 
tion in  detail  of  the  symptoms  of  this  trouble,  because  they  are  given 
under  the  head  of  cerebral  diplegia  or  birth  palsy.  The  only  difference 
between  ordinary  cerebral  diplegia  and  the  disease  under  present  con- 


SCELROSES,   DEGENERATIONS,    SYPHILIS 


281 


sideration  is  that  in  this  latter  form  there  are  no  marked  mental  defects; 
the  child  is  not  small  headed  and  idiotic,  nor  does  it  have  epilepsy  or  cra- 
nial nerve  palsy  or  hydrocephalus.  The  brain  seems  to  be  spared  except 
so  far  as  its  motor  functions  are  concerned.  It  is  convenient  to  separate 
this  type  of  disease  from  the  ordinary  spastic  cerebral  palsies  with  mental 
defect,  for  the  reason  that  the  future  of  these  cases  is  in  some  instances 
more  hopeful.  As  they  mature,  the  lateral  columns  occasionally  gain  in 
development  and  some  increase  in  the 
strength  and  control  of  the  limbs  is  ob- 
tained. I  base  this  statement  upon  the 
experience  of  others.  In  several  cases  of 
Little's  disease  at  the  age  of  fifteen  to 
twenty-five  which  I  have  seen,  there  has  been 
no  marked  improvement.  Mentally,  how- 
ever, these  patients  are  often  very  bright.  ^ 

Children  with  this  trouble  on  trying  to 
walk  are  obliged  to  cross  one  leg  in  front 
of  the  other  as  they  are  helped  along,  giving 
them  a  characteristic  ''cross-legged"  pro- 
gression. The  arms  are  less  affected  than 
the  legs.  The  facial  and  throat  muscles 
may  be  slightly  involved.  There  is  no 
pain.  In  some  cases  the  disability  increases 
as  the  child  grows  older,  owing  to  the 
greater  size  and  clumsiness  of  the  patient. 
The  arms  become  much  stiffened  and  con- 
tractured,  and  the  hands  are  flexed  so  that 
the  patient  can  neither  walk  nor  help  him- 
self. Epilepsy  and  mental  deterioration 
also  may  develop  at  the  time  of  puberty  or 
adolescence  but  they  do  not  belong  to  the 
typical  form. 

Prognosis. — ^The  mild  cases  that  learn  how  to  walk  and  can  use  the 
arms  and  hands  may  grow  up,  slowly  improving,  and  reach  a  good  age  and 
a  fair  degree  of  health.  The  severer  cases  rarely  reach  adolescence,  but 
grow  gradually  more  helpless  and  generally  succumb  to  some  intercurrent 
disease  before  they  are  twenty. 

Diagnosis. — -The  disease  is  distinguished  from  ordinary  cerebral 
diplegia  (birth  palsy)  due  to  brain  lesion  by  the  absence  of  epilepsy,  men- 
tal defects  and  microcephalus.     (See  Cerebral  Diplegia.) 


Fig.  127. — Little's  disease 
showing  adduction  of  thighs  and 
cross-legged  progression. 


1  It  is  due  to  American  neurology  to  say  that  Dr.  Seguin  as  long  ago  as  1879  said: 
"It  is  possible  that  tetanoid  paraplegia  in  young  children  may  be  due  to  deficient 
cerebral  development  and  consequently  agenesis  of  certain  tracts  of  the  cord." 


282  DISEASES    OF    THE    NERVOUS    SYSTEM 

From  compression  myelitis,  the  involvement  of  the  arms  and  the 
absence  of  pain  and  disturbance  of  sphincters  are  distinctive.  Hereditary- 
spastic  paraplegia  runs  in  families,  begins  at  the  fourth  or  fifth  year,  and 
involves  chiefly  the  legs. 

Treatment. — This  is  altogether  one  of  mechanics  and  attention  to 
nutrition.  The  limbs  must  be  persistently  massed;  tenotomies  should  be 
performed  so  as  to  straighten  the  legs;  constant  voluntary  effort  to  use 
the  stiffened  muscles  should  be  made.  Resection  of  certain  of  the  pos- 
terior roots  has  given  some  favorable  results.  Braces,  roller  crutches, 
etc.,  should  be  used.     Patience  is  often  greatly  rewarded  in  this  disease. 

THE  COMBINED  SCLEROSES 

By  the  combined  scleroses  is  meant  those  forms  of  degenerative  sclero- 
sis in  which  both  the  posterior  and  lateral  columns  are  involved. 

There  are  several  diseases  in  which  combined  sclerosis  exists.  They 
are: 

1.  Combined  scleroses  of  profoundly  anaemic  and  toxic  states  (Put- 
nam's type). 

2.  Hereditary  spinal  ataxia  (Friedreich's  ataxia). 

3.  Combined  scleroses  complicating  general  paresis. 

4.  Tabetic  form. 

There  are  many  cases  reported  in  literature  of  combined  scleroses,  but 
the  clinical  pictures  vary  very  greatly.  These  cases  are  probably  in  the 
most  part  forms  of  chronic  myelitis  or  multiple  sclerosis  with  ascending 
and  descending  degeneration.  Marie  has  shown  that  the  vascular  supply 
of  the  spinal  cord  is  such  as  rather  to  favor  the  development  by  extension 
of  sclerosis  in  the  lateral  and  posterior  columns  from  a  chronic  leptomen- 
ingitis, and  his  suggestion  that  many  of  these  cases  are  perhaps  of  syphil- 
itic origin  accords  with  my  experience  and  conviction.  Some  years  ago, 
Cowers  described  a  disease  that  he  called  ataxic  paraplegia,  the  lesion  in 
which,  he  believed,  lay  in  the  lateral  and  posterior  columns.  Most  of  the 
cases  which  belong  to  this  clinical  description  I  think  can  be  properly 
classed  either  with  the  cases  of  locomotor  ataxia,  of  multiple  sclerosis  or  of 
some  form  of  chronic  myelitis. 

THE  COMBINED  SCLEROSES  OF  PERNICIOUS  ,AN^MIA  AND  CACHECTIC 

STATES 

(Putnam^s  Type) 

This  form  of  disease  was  first  described  by  Dr.  J.  J.  Putnam,  later  by 
myself.  It  is  certainly  rather  common  in  this  country,  being  almost  as 
frequent  as  multiple  sclerosis. 


SCLEROSES,    DEGENERATIONS,    SYPHILIS  283 

Etiology. — The  disease  occurs  oftener  in  men.  Eleven  out  of  my 
twenty-three  cases  were  in  women. 

The  age  of  most  cases  is  between  50  and  65  (16  out  of  23),  and  next  to 
this  between  40  and  50  (5).  The  youngest  case  was  36  (Rothmann's). 
There  is  often  some  family  or  personal  neuropathic  history.  I  have 
reported  three  cases  occurring  in  one  family. 

The  disease  follows  acute  infections  like  influenza,  prolonged  diar- 
rhoeal  or  dysenteric  attacks,  and  serious  dietetic  errors.  One  patient 
had  a  malignant  tumor. 

The  most  important  cause  is  that  associated  with  severe  or  pernicious 
anaemia,  which  in  turn  is  attributed  to  gastro-intestinal  disturbance  and 
consequent  toxaemia.  Probably  some  intestinal  micro-organism  is 
behind  the  whole.  Syphilis  is  not  a  cause.  Often,  if  not  always,  how- 
ever, nervous  symptoms  develop  before  evidences  of  extreme  or  extended 
anaemia  are  present. 

Symptoms. — The  initial  nervous  symptom  is  nearly  always  a  persist- 
ent paraesthesia  of  the  feet  and  hands  associated  with  some  weakness  of 
the  part.  The  paraesthesia  is  of  the  stocking  or  glovetype  and  gradually 
ascends  the  legs  and  arms.  It  is  rather  sharply  limited.  The  tip  of 
the  tongue  and  nose  may  be  affected.  Following  this  there  is  a  good 
deal  of  ataxia,  with  some  loss  of  deep  sensibility,  and  this  symptom 
increases  with  the  loss  of  motor  power.  Tactile,  thermic  and  pain  anaes- 
thesias are  not  marked  until  late  in  the  disease,  but  the  patient  often  has 
severe  pains  in  the  back  and  limbs  and  often  complains  bitterly  of  his 
parasthesiae.  There  may  be  some  differentiation  of  sensibility  as  in 
syringomyelia.  With  the  weakness  of  the  legs  there  is  at  first  an  increase 
of  knee-jerks,  and  sometimes  ankle  clonus  and  rigidity,  so  that  the  patient 
shows  the  symptoms  of  ataxic  paraplegia.  Later  the  spasticity  may 
become  less  and  the  knee-jerks  disappear. 

When  the  arms  are  involved,  paraesthesia,  weakness,  awkwardness  and 
a  very  slight  anaesthesia  develop  and  progress.  The  mind  may  be  slightly 
weakened,  the  memory  becoming  defective  and  the  patient  emotional. 
The  cranial  nerves  are  not  often  involved,  though  optic  atrophy  has  been 
once  noted.  The  blood  presents  evidences  of  anaemia.  Usually  this  is 
secondary,  but  in  about  40  per  cent,  of  cases  there  are  the  typical  findings 
of  pernicious  anaemia.  It  should  be  noted  that  a  large  proportion  of  cases 
of  pernicious  anaemia  have  slight  involvement  of  the  spinal  cord  and  show 
some  acro-parsesthesia  and  motor  weakness,  but  do  not  develop  the  disease. 

The  disease  progresses  rather  rapidly,  though  hopeful  remissions  of  six 
to  twelvemonths  occur.  In  from  six  months  to  a  year,  if  there  is  no  re- 
mission, the  process  has  nearly  reached  its  height.  During  this  time  the 
patient  emaciates,  marked  anaemia  or  pernicious  anaemia  sets  in.  The  skin 
is  sallow  and  pale,  and  pigmentation  is  seen.     Diarrhoea  occurs  at  times. 


284 


DISEASES    OF    THE    NEKVOUS    SYSTEM 


The  bladder  becomes  weak  and  retention  of  urine  follows;  the  control  of 
the  rectum  is  eventually  lost,  and  the  patient  lies  bed-ridden  with  paraly- 
sis and  contractures  of  the  lower  limbs.  The  arms  do  not  become  so 
badly  paralyzed. 

Prognosis. — Death  usually  occurs  in  about  two  years  in  the  progress- 
ive cases.  It  may  be  prolonged  to  three  years,  and  I  have  found  that  if 
the  trouble  is  recognized  early  the  process  may  be  checked.  The  progno- 
sis is  better  in  older  patients. 

Pathology. — ^The  disease  is  a  toxic  one,  but  whether  due  to  the  failure 
of  some  glandular  tissue  of  the  body  to  act  or  to  infection  or  poison  is  not 
known.  As  the  disease  belongs  to  the  degenerative  period  of  life,  it  may 
fairly  be  supposed  that  in  some  cases  the  blood-making  organs  undergo 
premature  decay  and  that  the  nerve  centres  are  poisoned  in  consequence; 


Fig.  128. — ^Lesion  of  posterior  column  in  pernicious  anaemia. 


or  the  intestinal  tract  may  be  the  origin  of  the  poison  since  in  the  severe 
anaemias  there  is  great  atrophy  of  the  mucous  membranes.  The  process 
is  classed  as  chronic  degenerative  myelitis  by  some  writers,  but  I  see 
no  reason  for  regarding  it  as  a  true  inflammation. 

As  to  the  location  of  the  trouble,  the  posterior  columns  of  the  spinal 
cord  are  the  parts  first  and  most  involved  (Fig.  128).  The  process  espec- 
ially involves  the  postero-median  parts.  It  appears  to  start  in  certain 
foci  in  the  lower  dorsal  or  cervical  cord,  and  to  spread  thence.  New  foci 
apparently  develop  as  the  disease  progresses;  the  lateral  columns  are  also 
severely  affected,  and  especially  the  crossed  pyramidal  tracts  (Fig.  130). 
The  other  columns  are  involved,  but  less  regularly  and  completely. 
The  lower  dorsal  and  lower  cervical  levels  of  the  cord  are  especially 
selected.     The    anterior   horns    are    finally   involved,    but    the    change 


SCLEROSES,    DEGENERATIONS,    SYPHILIS 


285 


)J+eili<M 


JD  /o 


here  comes  later.  Finally,  there  may  be  actual  softenings  in  the  cord,  pro- 
ducing cavities  (Fig.  130).  Sometimes  the  pathological  process  is  irregu- 
larly diffuse  and  not  systemic.  The  blood-vessels  are  somewhat  affected 
with  hyaline  degeneration,  but  I  am  unable  to  say  how  important  a  factor 
this  is.  The  walls  are  thickened;  there  are  in  places  dilatations  and 
hemorrhages,  and  in  other  places  collapsed  vessels.  There  is  no  evidence 
of  inflammatory  reaction.  The  men- 
inges are  not  involved,  nor  are  the 
anterior  and  posterior  roots  much  af- 
fected. Examinations  of  the  per- 
ipheral nerves  (Rothmann)  and  of  the 
brain  have  been  negative. 

Diagnosis. — The  disease  is  easily 
distinguished  from  locomotor  ataxia 
by  the  absence  of  syphilitic  history, 
the  rapid  onset,  the  anaemia,  the  pe- 
culiar progressive  acro-parsesthesia, 
the  motor  weakness,  the  absence  of 
ocular  symptoms  and  of  lightning 
pains.  There  is  usually  also  at  first 
an  exaggeration  of  the  reflexes.  The 
steady  and  rapid  progress  of  the  mal- 
ady is  also  most  characteristic. 

Multiple  neuritis  is  excluded  by 
the  slow  onset,  the  marked  ataxia, 
the  absence  of  muscular  wasting  and 
of  tenderness  and  pain,  and  the  de- 
velopment of  bladder  and  rectal 
symptoms. 

One  of  my  cases  presented  such 
a  marked  differentiation  of  cutaneous 
sensations  that  I  believed  it  to  be  one 
of  syringomyelia.  The  necropsy 
showed  a  cavity  in  the  cervical  cord 
due  to  softening,  and  in  a  measure  ex- 
plained, if  it  did  not  justify,  the  diagnosis.  The  steady  and  rapid  prog- 
ress of  the  symptoms  ought  to  exclude  such  a  diagnosis. 

The  existence  of  marked  anaemia,  and  especially  of  pernicious  anaemia, 
is,  taken  with  acro-paraesthesia,  ataxia,  paralysis  and  rapid  course,  pathog- 
nomonic. 

The  essential  nature  of  this  process  is  a  parenchymatous  degeneration, 
affecting  apparently  the  axon-tissue  first.  The  same  poison  which 
causes  pernicious  anaemia  does  the  work  here,  only  it  may  affect  the  nerv- 


-O/ 


^/y. 


Fig.  129. — Combined  sclerosis  of 
toxic  origin,  showing  location  of  degen- 
eration of  original  foci  of  disease. 


286  DISEASES    OF    THE    NEEVOUS    SYSTEM 

ous  centres  before  causing  a  true  essential  anaemia.     It  seems  even  as  if 
in  some  cases  the  neural  change  came  first. 

Treatment. — The  use  of  arsenic  sometimes  is  helpful  and  brings  on 
remissions  in  those  cases  associated  with  anaemia.  Intestinal  antiseptics 
and  colon  washings,  abundant  food,  salvarsan  injections,  transfusions, 
fresh  air  and  tonic  medication  are  the  measures  indicated. 


Fig.  130. — The  spinal  cord  in  combined  sclerosis  from  pernicious  ansemia,  dorsal 
region.  The  columns  of  GoU,  crossed  pyramidal  tracts,  and  cerebellar  tracts  are 
affected. 

HEREDITARY  SPINAL  ATAXIA 

{Friedreich's  Ataxia) 

There  are  three  forms  of  hereditary  or  congenital  spinal  and  cerebellar 
defects  which  should  be  grouped  together:  They  are:  (1)  Hereditary 
spinal  ataxia,  or  Friedreich's  ataxia:  (2)  hereditary  cerebellar  ataxia; 
and  (3)  hereditary  spastic  paraplegia.  They  are  quite  similar  in  cause 
and  mode  of  development.  The  difference  in  symptom  depends  upon 
the  fact  that  the  defect  exists  in  the  one  case  mainly  in  the  posterior  and 
lateral  columns  of  the  cord  in  the  second  in  the  cerebellum,  and  in  the 
third  mainly  in  the  lateral  columns. 

Friedreich's  ataxia,  the  most  common  of  all  the  forms,  is  a  chronic 
degenerative  disease  mainly  affecting  the  posterior  and  lateral  columns  of 
the   cord. 

Clinically,  the  disease  is  characterized  by  ataxia  beginning  in  the 
lower  limbs  and  gradually  involving  the  upper  limbs  and  the  organs  of 
speech.  Curvature  of  the  spine,  talipes,  and  finally  paralysis  and  con- 
tractures appear. 

Etiology. — ^The  fundamental  factor  in  predisposition  is  an  inherited 
or  connate  lack  of  development  of  the  spinal  cord,  more  particularly  of 
the  posterior  columns  and  pyramidal  tracts.  This  condition  is  inherited 
directly  sometimes,  but  indirectly  as  a  rule ;  that  is  to  say,  the  parents  or 
other  members  of  the  family  usually  show  simply  a  neurotic  history,  and 
it  is  in  only  a  minority  of  cases  that  there  is  a  history  of  ataxia  in  the  direct 
line  of  ancestry. 


SCLEROSES,    DEGENERATIONS,    SYPHILIS  287 

The  more  frequent  condition  is  this :  the  parents  or  grandparents  have 
some  neuroses,  such  as  insanity,  inebriety  or  great  nervous  irritabihty; 
then  the  ataxia  occurs  in  the  children  of  the  next  generation.  Sometimes 
in  a  single  family  the  uncles  and  nephews  or  cousins  may  be  found  to  have 
the  disease.  Hence  the  name  "family  ataxia,"  used  by  some  writers. 
There  are  a  good  many  cases  in  which  the  parents  were  apparently  per- 
fectly sound  and  healthy.  The  parents  rarely  have  locomotor  ataxia, 
though  this  has  been  observed  in  a  few  cases. 

Syphilis  in  the  ascendants  is  an  element  in  some,  probably  in  many 
cases.  Habitual  intemperance  in  parents  is  perhaps  sometimes  a  factor; 
much  more  rarely  consanguinity  and  tuberculosis  act  as  predisposing 
causes  of  degeneration.  More  cases  have  been  observed  in  America 
than  in  any  other  country;  while  the  fewest  have  been  reported  from 
France. 

The  disease  develops  at  about  the  time  of  puberty,  most  cases  occur- 
ring between  the  ages  of  six  and  fifteen  years.  It  is  not  very  rare,  how- 
ever, for  symptoms  to  develop  even  in  infancy,  though  some  of  the  cases 
reported  at  this  time  were  probably  of  a  syphilitic  character. 

In  a  given  family  the  disease,  as  a  rule,  strikes  the  older  members 
first,  but  the  younger  members  are  attacked  at  a  relatively  earlier  age. 
The  most  typical  time  of  development  is  a  rather  late  one;  i.e.,  after 
twelve  years  of  age.  The  disease  may  come  on  after  maturity.  In 
American  cases  the  age  of  development  of  the  disease  has  been  rather 
earlier  than  the  average. 

The  male  sex  slightly  predominates,  its  proportion  being  about  60 
per  cent.  In  America  the  female  sex  has,  however,  been  more  affected 
(3  to  2). 

The  patients,  as  a  rule  are  the  children  of  the  laboring  and  agri- 
cultural classes.  They  have  been  found  in  the  country  oftener  than 
in  crowded  cities.  The  families  have  often  been  large,  but  this  is  not 
always  the  case,  especially  in  American  cases.  Usually  the  disease 
appears  after  infectious  fevers,  such  as  diphtheria,  variola  and  typhoid. 

Symptoms. — The  child  is  first  noticed  to  have  an  uncertainty  in 
the  gait  and  some  feebleness  in  the  lower  limbs.  These  symptoms 
gradually  increase  until  they  interfere  seriously  with  progression,  and 
force  him  in  two  or  three  years  to  leave  off  active  play.  With  this  there 
may  be  some  slight  pains  or  numbness  in  the  lower  limbs,  and  an  examina- 
tion will  show,  within  a  year  or  earlier,  that  the  knee-jerk  is  gone.  After 
five  or  six  years  the  arms  become  affected  with  inco-ordination,  and  a 
little  later  bulbar  symptoms,  such  as  thick  or  scanning  speech,  and  often 
nystagmus,  appear.  These  bulbar  symptoms  may  be  very  much  delayed. 
During  this  time  the  patient  suffers  little  pain  or  anaesthesia  and  has  no 
trouble  with  the  bladder  or  rectum.     Vertigo  and  hea,dache  are  often 


288 


DISEASES    OP    THE    NERVOUS    SYSTEM 


present.  Dorsal  flexion  of  the  toes,  talipes  varus  or  some  other  form  of 
clubfoot,  and  lateral  curvature  of  the  spine  are  often  observed  (Fig. 
131).  Oscillation  of  the  head  and  choreiform  or  inco-ordinate  move- 
ments of  the  extremities  may  develop.  As  the  disease  progresses  the 
legs  become  weaker,  and  finally  paraplegia,  with  contractures  and  mus- 
cular wasting,  sets  in.  The  intelligence  is  sometimes  diminished.  The 
disease  makes  slow  progress;  often  it  remains  almost  at  a  standstill  for 
years,  and  the  patients  usually  die  of  some  intercurrent  disease,  such  as 
phthisis  or  an  infectious  fever. 

Among  the  rarely  observed  symptoms  are  tremor  of  the  hands  and 

head,  spasms,  sluggish  pupils,  tachy- 
cardia, profuse  sweats,  impotence, 
slight  vesical  incontinence,  fragilitas 
ossium.  Many  of  these  symptoms 
occur  only  late  in  the  disease.  When 
there  is  marked  involvement  of  the 
cranial  nerves,  the  disease  may  be  put 
down  as  a  cerebellar-spinal  trouble. 
The  major  and  essential  symp- 
toms are:  (1)  ataxia,  beginning  in  the 
lower  limbs  and  extending  to  the 
arms  and  tongue;  peculiar  rolling, 
ataxic  gait;  (2)  disturbances  of 
speech;  (3)  talipes  and  spinal  curva- 
tures; (4)  gradual  development  of 
paraplegia;  (5)  loss  of  knee-jerk;  (6) 
absence  of  cutaneous  anaesthesia,  of 
bladder  troubles,  of  eye  troubles  ex- 
cept nystagmus,  and  of  severe  pains; 
(7)  the  development  of  the  foregoing  at  about  the  time  of  puberty. 

Diagnosis. — The  disease  must  be  distinguished  from  multiple  scle- 
rosis of  spinal  type,  and  from  cerebellar  ataxia  and  tumors.  The  family 
history  is  usually  of  help.  The  disease  begins  earlier  in  life  than  does 
multiple  sclerosis.  The  speech  disturbances,  nystagmus,  paraesthesise, 
pallor  of  the  optic  discs,  intention  tremor,  and  exaggerated  reflexes  also 
serve  to  distinguish  multiple  sclerosis.  The  differentiation  from  heredi- 
tary cerebellar  ataxia  is  not  important  as  the  two  diseases  are  really  the 
same.  The  general  symptoms  of  brain  tumor  are  not  present  in  cerebellar 
ataxia. 

Pathology. — The  lesions  of  importance  are  found  in  the  spinal  cord 
and  medulla  only.  The  cord  is  usually  small,  flattened  and  apparently 
congenitally  imperfect  in  development.  In  some  cases  two  central 
canals  have  been  seen.     A  sclerosis  exists  throughout  the  whole  length 


Fig. 


131. — Friedreich's   ataxia   showing 
late  deformities  of  feet. 


SCLEROSES,    DEGENERATIONS,    SYPHILIS 


289 


of  the  posterior  and  lateral  columns,  sometimes  extending  to  the  anterior 
columns  (Fig.  133).  The  sclerosis  is  most  marked  in  the  postero-median 
columns,  which  are  eventually  affected  in  toto.  The  postero-external 
column  is  less  involved  and  there  is  often  a  narrow  strip  of  healthy  tissue 
between  the  posterior  horn  and  the  sclerosed  area,  also  between  the 
posterior  gray  commissure  and  the  diseased  parts.  The  posterior-column 
sclerosis  is  usually  most  marked  in  the  lumbar  region.  In  the  lateral 
columns  the  sclerosis  always  affects  most  the  crossed  pyramidal  tracts. 
The  direct  cerebellar  tracts  and  the  so-called  ascending  antero-lateral 
tract  are  diseased  in  some  cases,  but  apparently  not  in  all.  In  a  few 
instances  the  anterior  median  columns  are  involved.  A  zone  of  healthy 
tissue  is  often  found  between  the  sclerosed  pyramidal  tracts  and  the  pos- 
terior horn.  There  are  no  important  changes  in  the  gray  matter  except 
a  secondary  atrophic  process.  Some  chronic  leptomeningitis,  especially 
on  the  posterior  surface,  has  been  noted.     The  medulla  shows  some  traces 


Fig.  132. — Friedreich's  ataxia. 


of  extension  of  the  sclerosis,  but  the  involvement  of  the  cells  of  the  hypo- 
glossal nucleus  is  probably  the  most  significant  change.  The  brain  ex- 
hibits no  changes  of  importance  in  relation  to  the  symptomatology  of  the 
disease.  The  posterior  nerve-roots  are  extensively  sclerosed,  the  anterior 
roots  less  so,  and  the  peripheral  nerves  show  some  degenerative  changes. 
The  peripheral  nerves  are  much  less  involved  than  in  tabes  dorsalis. 
It  is  asserted  that  the  sclerosis  in  the  cord  is  really  a  neuroglia  prolifera- 
tion— a  gliosis — and  there  is  no  doubt  a  large  amount  of  neuroglia  pro- 
liferation in  the  diseased  areas. 

Course  and  Prognosis. — The  disease  is  a  progressive  one,  though  it 
may  be  stationary  for  a  long  time  and  may  even  show  temporary  improve- 
ment. The  longest  period  of  duration  of  the  disease  on  record  is  forty- 
six  years  and  the  shortest  two  years,  the  average  being  fifteen  or  twenty 
3^ears.  Death  occurs  from  some  intercurrent  disorder  or  from  bulbar 
complications. 

19 


290 


DISEASES    OF    THE    NERVOUS    SYSTEM 


Treatment. — A  quiet  life,  good  food  and  favorable  hygienic  surround- 
ings are  the  main  therapeutic  helps.     Arsenic  and  various  nerve  tonics 


r= 


.^ 


#l^% 


Fig  133.-- Spinal  cord  in  a  long-standing  case  of  hereditary  ataxia. 

may  be  of  temporary  benefit.     If  blood  tests  give  evidence  of  syphilis 
in  the  patient  or  parent,  salvarsan,  mercury  and  iodide  are  indicated. 


SCLEROSES,   DEGENERATIONS,    SYPHILIS  291 

A  course  of  mercurial  injections  or  inunctions  is  advisable  in  the  early 
stages. 

Hereditary  Spastic  Paraplegia  is  an  extremely  rare  malady  resembling 
in  general  course  the  adult  form  of  lateral  sclerosis  (p.  279). 

HEREDITARY  CEREBELLAR  ATAXIA 

This  is  a  disease  so  akin  to  hereditary  ataxia  that  some  writers  think 
it  useless  to  try  and  distinguish  them.  I  can  only  say  that  in  my  ex- 
perience the  disease  sometimes  shows  itself  mostly  in  cerebellar  and 
cranial  nerve  symptoms. 

The  first  symptom  is  shown  in  a  disturbance  of  the  gait.  This  is 
indicated  by  clumsiness  and  stumbling  and  by  a  tendency  to  rolling 
and  pitching  like  a  drunken  man.  There  are  inco-ordination  and  jerki- 
ness  in  the  movements  of  the  arms  and  sometimes  choreic  movements. 
The  patient  also  has  oscillation  and  jerky  movements  of  the  head. 
When  lying  down  the  inco-ordination  is  very  much  lessened.  The  speech 
is  hesitating,  ataxic  and  explosive.  The  eyes  show  jerky  movements 
somewhat  like  those  of  nystagmus.  An  important  symptom  in  some  cases 
is  the  development  of  optic  neuritis  followed  but  not  always  by  optic 
atrophy  and  blindness.  The  knee-jerks  are  usually  exaggerated.  The 
patient  has  no  anaesthesia  and  suffers  little  pain,  although  he  may  have 
some  headache.  There  is  no  disturbance  of  the  sphincters.  Mentally, 
the  patients  are  usually  somewhat  deficient,  becoming  eventually  either 
simply  childish  or  actually  demented.  The  malady  progresses  and  ends 
like  that  of  the  spinal  type. 

Pathological  Anatomy .-^The  few  autopsies  w^hich  have  been  made 
show  an  atrophy  of  the  cerebellum.  In  some  cases  this  is  macroscopic, 
the  cerebellum  being  reduced  to  one-half  or  one-third  its  size.  In  other 
cases  there  is  no  naked-eye  change,  but  there  is  found  microscopically 
an  atrophy  of  the  cortical  matter. 

Diagnosis.- — -In  the  cerebellar  type,  the  distinguishing  features  are 
the  presence  of  the  knee-jerks,  the  absence  or  late  occurrence  only  of  a 
spastic  or  ataxic  paralysis,  the  presence  of  speech  defects,  of  nystagmus 
and  jerky  tremors  and  of  the  group  of  other  special  cerebellar  symptoms; 
also  the  occurrence  at  times  of  an  optic  atrophy.  In  the  spinal  form 
the  early  and  more  prominent  paraplegic  symptoms  develop,  with 
deformities  of  the  feet,  while  there  is  a  late  involvement  only  of  the 
cranial  nerves. 


CHAPTER  XIV 

THE  PROGRESSIVE  MUSCULAR  ATROPHIES  AND 
MUSCULAR  DYSTROPHIES 


The  peripheral  motor  neurons  of  the  spinal  cord,  and  their  terminal 
end  organs,  the  muscles,  form  a  trophic  unit,  and  the  same  degenerative 
disease  may  attack  either  end  or  any  part  of  this  physiological  mechanism. 
There  is  a  clinical  and  pathological  relationship  between  the  different 
spinal  and  muscular  types  of  atrophies.  But  there  are  sufficient  differ- 
ences, also,  as  to  oblige  us  for  convenience  sake  to  make  certain  classifica- 
tions. Thus  those  disorders  which  attack  chiefly  and  first  the  anterior 
horn  cells  are  called  progressive  muscular  atrophies;  those  disorders 
attacking  first  the  muscle  tissue  and  its  nerves  are  called  progressive 
muscular  dystrophies.  The  progressive  muscular  atrophies  of  central 
origin  may  attack  the  motor-nerve  cells  of  the  eye,  of  the  throat  and 
lips,  of  the  upper  or  lower  spinal  cord.  In  accordance  with  the  level 
affected,  the  disease  has  received  different  names.  Sometimes  the 
pyramidal  tracts  of  the  spinal  cord  are  first  and  most  involved,  and 
later  the  peripheral  motor  neuron  is  affected.  This  has  furnished 
excuse  for  another  type.  Then,  again,  while  most  cases  of  muscular 
atrophy  are  acquired,  there  are  types  which  are  hereditary.  Thus  we 
find  the  disease  classified  as  follows: 


Progressive  mus- 
cular atrophies. 


Spinal  form. 


Bulbar  form. 

Mesencephalic 
form. 


j  Duchenne-Aran  or  common  type. 

j  Luetic  type. 

[  Hereditary  types: 

Infantile. 

Adult. 

Charcot-Marie-Tooth. 

f  Progressive  bulbar  paralvsis. 

I 

I 

■|  Progressive  ophthalmoplegia. 


Upper  neuron  form      [  Amyotrophic  lateral  sclerosis. 

The  progressive  muscular   dystrophies  have  also  been  much  sub- 
divided, but  they  are  essentially  the  same  disease,  as  will  be  seen  later. 

Of  the  above  progressive  atrophies,  I  have  already  described  ophthal- 
moplegia (page  100). 

292 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES 


293 


PROGRESSIVE  MUSCULAR  ATROPHY 

{Progressive  Spinal  Amyotrophy;  Duchenne-Arati' s  Disease) 

This  is  a  disease  characterized  by  a  slow,  progressive  atrophy  of  the 
muscles  of  the  extremities  and  trunk,  with  consequent  paralysis,  not 
accompanied  by  any  notable  sensory  disturbance,  and  due  to  a  pro- 
gressive atrophy  of  the  lower  motor  neurons  in  the  spinal  cord.  In 
the  more  typical  and  common  form  (Duchenne-Aran's)  the  disease 
begins  in  the  upper  extremity. 

Etiology. — The  disease  affects  persons  in  the  middle  period  of  life 
(twenty-five  to  forty-five).  The  extremes  are  fourteen  and  seventy 
years.  It  is  more  frequent  in  males.  Heredity  is  rarely,  if  ever,  a 
direct  factor.     Great  mental  sti-ain,  exposure,  traumatism,  excessive  use 


Fig.  134. — Showing:  1.  Segment  of  spinal  cord  with  motor  neuron,  end  brush, 
and  lateral  tracts,  the  parts  affected  in  progressive  muscular  atropliies;  and  2,  the 
muscle  and  its  nerves,  the  parts  affected  in  progressive  muscular  dystrophies. 

of  certain  groups  of  muscles,  acute  infectious  diseases — especiallj^ 
typhoid — childbirth,  acute  rheumatism,  and  lead  poisoning  are  among 
the  causes.  All  three  types  of  atrophy  may  be  caused  by  syphilis, 
and  hence  the  disease  may  occur  in  locomotor  ataxia.  Usually,  however, 
syphilis  causes  an  atrophy  running  a  rather  special  course. "^ 

1  Among  seventy-two  cases,  four-fifths  were  in  males.  Spyhilis  was  present  in  about 
one-fifth  of  the  cases.  With  regard  to  age,  I  have  seen  two  cases  beginning  as  early  as 
the  twelfth  year,  of  the  Duchenne-Aran  variety,  in  the  most  characteristic  form.  In 
one  case,  which  I  have  now  watched  from  the  time  it  began,  at  the  twelfth  year,  to  the 
present  time,  the  patient  now  being  twenty-four,  the  disease  was  arrested  after  about 
four  years  of  progress,  the  patient  being  left  with  simply  an  atrophy  of  the  left  forearm, 
in  the  muscles  of  the  ulnar  distribution.  My  oldest  patient  was  one  of  a  perfectly 
typical  arm  type  of  atrophy  seen  with  Dr.  J.  Arthur  Booth,  occurring  in  a  physician 
aged  seventy-two,  but  beginning,  probably,  before  his  seventieth  year.  The  period 
during  which  the  greatest  number  of  cases  were  seen  was  that  between  the  thirtieth 
and  fortieth  years,  and  next,  between  that  of  forty  and  fifty.  In  cases  of  bulbar 
paralysis  the  age  of  fifty-three  seems  to  be  a  singularly  serious  year.  I  note  the  occur- 
rence of  six  cases  at  about  that  period  of  time,  among  twelve  in  all.  There  were 
about  five  times  as  many  cases  among  males  as  among  females,  but  this  does  not 
apply  to  all  types  of  the  disease.  In  the  bulbar  cases  there  were  more  women,  the 
proportion  being  8  to  4. 

Among  the  exciting  causes,  by  far  the  most  frequent  is  that  of  some  form  of  strenu- 
ous occupation.     Workmen  who  had  to  do  very  heavy  work,  athletes  or  professional 


294 


DISEASES    OF    THE    NERVOUS    SYSTEM 


Symptoms. — The  patient  suffers  at  first  from  slight  rheumatoid 
pains  in  the  shoulder  or  arm,  associated  with  some  feelings  of  numbness 
and  weariness.  Muscular  wasting  then  begins  to  appear  in  the  intrinsic 
muscles  of  one  hand.  The  adductor  longus  polhcis  is  very  early  affected 
as  are  the  thenar  muscles  and  the  interossei.  The  atrophy  spreads  from 
muscle  to  muscle,  and  does  not  follow  the  distribution  of  nerves,  al- 
though the  ulnar-nerve  supply  is  most  seriously  disordered.  The 
ball  of  the  thumb  becomes  flattened,  and  the  patient  cannot  abduct 
or  flex  it  well.  When  the  radial  interossei  are  reached  the  forefinger 
cannot  be  abducted,  and  this  is  often  an  early  sign.  The  disease  gradu- 
ally extends  upward,  attacking  the  flexors 
more  than  the  extensors  of  the  wrist,  then 
the  upper  arm  and  shoulder,  affecting 
abduction  and  flexion  of  forearm  espe- 
cially. Meanwhile  the  hand  has  become 
thin  and  flattened,  flexion  of  wrist  and 
extension  of  fingers  are  lost  (owing  to  the 
more  special  involvement  of  the  ulnar 
nerve)  and  a  characteristic  ''griffin- 
claw"  appearance  results.  After  a  time 
(three  to  nine  months)  the  other  arm  be- 
gins to  be  affected.  Occasionally  there 
is  a  temporary  remission. 

In  a  few  cases  the  atrophy  begins 
first  in  the  shoulders  and  arms,  attack- 
ing the  deltoid,  biceps  and  triceps,  then 
extending  downward  to  the  hands.  This 
constitutes  the  "upper-arm  type." 

If,  as  is  usually  the  case,  the  disease 
continues  to  progress,  it  passes  from  the 
shoulder  girdle  to  the  deep  muscles  of  the  back,  then  downward,  in- 
volving successively  the  thigh  muscles,  the  glutei,  the  crural  extensors 
and  abductors  being  oftenest  chosen.  The  leg  muscles  may  be  finally, 
involved,  but  they  usually  escape.  The  disease  as  it  descends  continues 
its    progress   in   the    trunk,    involving   the   intercostals.     It  slowly  as- 


FiG.  135. — Showing    wasting    of 
hands  in  muscular  atrophy. 


contortionists  were  among  the  victims,  and  in  the  cases  of  bulbar  paralysis,  there  was 
several  times  a  history  of  the  patients  being  very  great  and  excessive  talkers.  Lead, 
as  a  cause  of  paralysis,  does  not  seem  to  me,  after  all,  as  important  a  factor  as  has  been 
supposed.  It  could  be  blamed  for  the  disease  in  not  over  five  cases,  and  not  certainly 
in  all  of  these.  Several  of  my  patients  were  very  heavy  users  of  tobacco,  but  I  fancy 
this  was  only  a  coincidence.  Two  patients  had  in  infancy  a  previous  attack  of  polio- 
myelitis. In  one  case  there  was  a  very  distinct  history  of  an  acute  infection  by  dengue  ; 
it  is  not  improbable  that  other  cases  have  followed  an  acute  infection.  On  the  whole 
the  dominant  causes  are  an  occupation  strain,  syphilis,  and  some  inherited  weakness  of 
the  affected  neurones. 


MUSCULAR  ATROPHIES  AND  DYSTROPHIES  295 

cends  the  neck  also,  and  finally  leads  to  a  paralysis  of  the  diaphragm, 
or  a  bulbar  palsy  may  set  in. 

It  will  be  seen  that  the  ordinary  course  of  the  disease  is  from  the 
lower-arm  muscle  groups  (ulnar  and  median)  up  to  the  shoulder  group 
(middle  cervical  nerves),  then  down  through  the  dorsal  and  lumbar 
nerves,  rarely  reaching  the  sacral  groups,  then  up.  In  very  rare  cases 
it  begins  in  the  legs  and  ascends. 

Along  with  the  wasting  there  are  a  corresponding  weakness  and 
paralysis,  but  the  paralysis  is  the  result  of  the  atrophy  and  does  not 
precede  it.  Fibrillary  twitchings  of  the  muscles  occur;  the  idiopathic 
muscular  contraction  caused  by  striking  it  a  blow  is  often  marked; 
myoid  tumors  are  easily  brought  out.  In  some  cases  the  muscles  are 
flaccid  and  toneless,  and  the  deep  reflexes,  knee-jerk,  and  arm-jerk 
disappear  early  (atonic  atrophy),  but  in  most  cases  the  irritability  and 
tonicity  of  the  muscles  are  increased,  the  knee-jerks  exaggerated,  and 
we  have  tonic  atrophy.  This  condition  may  be  so  marked  as  to  make  it 
resemble  a  special  chnical  type  of  progressive  atrophy  known  as  amyo- 
trophic  lateral  sclerosis. 

The  electrical  irritability  of  the  muscles  gradually  lessens  to  both 
galvanic  and  faradic  currents,  but  no  marked  qualitative  changes  occur 
at  first.  Eventually  we  may  get  partial  degeneration  reactions,  but 
these  occur  late  in  the  disease,  unless  this  runs  a  very  rapid  course, 
when  fairly  typical  degeneration  reactions  may  be  got  early. 

In  typical  cases  of  progressive  muscular  atrophy  there  is  no  anaes- 
thesia, cutaneous  or  deep,  and  when  such  symptoms  develop  the  presence 
of  peripheral  disease  or  of  syringomyelia  or  spinal  tumor  must  be  sus- 
pected. The  patients  may  suffer  from  rheumatic-like  pains  and  from 
parsesthesias. 

The  affected  parts  often  show  excessive  sweating  and  congestion  and 
evidence  of  vasomotor  disturbance.  This  may  involve  the  face  on  one 
or  both  sides;  one  pupil  may  be  larger  than  the  other,  due  to  irritation  of 
the  cilio-spinal  centre.  The  iris  reflex,  however,  is  preserved,  and  the 
optic  nerve  is  never  involved. 

The  sexual  power  is  often  weakened,  but  the  sphincters  are  not 
attacked.  The  urine  shows  variations  in  the  amount  of  urea.  There 
is  usually  an  increase  of  lime  salts. 

Complications. — The  most  common  complication  is  an  extension  of 
the  process  to  the  medulla,  causing  disturbance  of  speech  and  swallow- 
ing (bulbar  paralysis).  Muscular  atrophy  compHcates  locomotor  ataxia, 
but  is  rarely  comphcated  by  it.  An  apparently  typical  and  flaccid 
atrophy  may  develop  spasticity  and  signs  of  involvement  of  the  pyramidal 
tracts;  in  other  words,  it  may  turn  out  to  be  an  upper  neuron  type  or 
amyotrophic  lateral  sclerosis. 


296  DISEASES    OF    THE    NERVOUS    SYSTEM 

Course  and  Duration. — The  disease  usually  progresses  steadily  until 
it  has  reached  an  advanced  stage,  when  it  may  stop.  Remissions  may 
occur  early,  however,  and  even  some  improvement  take  place;  the 
disease  then  ordinarily  progresses  again.  It  lasts  from  two  years  to 
thirty  or  more,  but  on  the  average  not  over  ten  or  twelve  years.  Death 
usually  occurs  from  pulmonary  disease,  owing  to  the  weakness  of  the 
respiratory  muscles.  Sometimes  the  extension  to  the  medulla  and  in- 
volvement of  the  muscles  of  deglutition  and  of  the  larynx  are  the  cause 
of  death. 

Pathology. — The  primary  anatomical  change  is  a  degenerative  atrophy 
of  the  neurons  of  the  central  parts  and  anterior  horns  of  the  gray  matter 
of  the  spinal  cord.  The  atrophy  gradually  extends  and  involves  the  whole 
anterior  horn.  It  also  extends  vertically,  first  down,  then  up.  Consecu- 
tive to  this  there  is  atrophy  of  the  anterior  roots,  peripheral  nerves 
and  the  muscles.  The  disease  begins  in  the  deeper  parts  of  the  anterior 
cornua,  involving  the  central  and  median  groups  of  cells.  These  are 
more  concerned  in  nutrition  and  in  the  finer  muscular  movements  of  the 
extremities.  Hence  atrophy  always  precedes  or  at  least  keeps  pace  with 
paralysis.  The  levels  affected  are  the  lower  cervical  and  upper  dorsal; 
but  if  the  disease  is  extensive  the  dorsal,  lumbar  and  sacral  cord  are  also 
involved.  The  affected  part  is  nearly  free  from  nerve-cells,  and  those 
present  are  atrophied,  their  processes  are  short  or  absent,  and  the  cell 
has  lost  its  angular  appearance.  Sclerotic  and  pigmentary  changes  are 
observed.  The  neuroglia  and  connective-tissue  cells  are  increased  in 
number,  but  there  are  no  marked  changes  in  the  blood-vessels,  though 
these  may  be  much  dilated.  There  is  often  some  degeneration  of  the 
lateral  columns.  It  is  confined  chiefly  to  the  pyramidal  tracts,  but  ex- 
tends somewhat  anteriorly  into  the  mixed  lateral  column.  It  does  not 
affect  the  cerebellar  or  ascending  lateral  tracts.  The  anterior  columns 
may  be  slightly  affected.  The  posterior  horns,  columns  and  roots  are 
normal. 

The  affected  muscles  show  various  degrees  of  degeneration.  They 
are  pale  and  streaked  with  yellow,  due  to  fatty  deposits.  Some  fibres 
may  be  simply  narrow  and  shrunken;  others  have  lost  their  striation 
and  become  granular  from  deposit  of  fat  globules  or  degenerated  muscle 
elements;  other  fibres  have  lost  their  striations  and  appear  as  if  filled 
with  a  homogeneous,  glassy-looking  substance  containing  a  few  fat 
granules  (vitreous  degeneration) ;  others  show  a  longitudinal  striation. 
The  interstitial  connective  tissue  is  increased  and  in  places  has  taken  the 
place  entirely  of  the  muscles.  The  capillaries  and  small  vessels  are  dis- 
tended. Healthy  fibres  may  be  seen  among  the  diseased.  Changes  have 
been  found  in  the  sympathetic  nervous  system,  but  they  are  unimportant. 

The  diagnosis  has  to  be  made  from  the  progressive  muscular  dys- 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES  297 

trophies,  chronic  poliomyelitis  anterior,  syringom^-elia,  neuritis  and 
neuritic  family  atrophy. 

In  the  muscular  dystrophies  there  is  commonly  a  history  of  heredity; 
the  disease  begins  usually  in  childhood  or  adolescence.  It  attacks  the 
lower  limbs  oftener;  it  is  slower  in  progress  and  the  two  sides  are  affected 
at  the  same  time;  there  are  no  fibrillary  contractions,  and  the  degeneration 
reaction  does  not  occur  till  very  late. 

Chronic  spinal  atrophy  or  chronic  (subacute)  anterior  poliomyelitis 
is  usually  due  to  sj-philis.  It  begins  rather  suddenly  and,  having  reached 
its  height,  does  not  progress,  but  remains  stationary  or  improves  for  a 
time.  The  paralj'sis  occurs  first,  the  wasting  follows.  It  affects  groups 
of  muscles  physiologicall}^  related  more  strictly  than  does  progressive 
muscular  atrophy.  Lumbar  puncture  gives  positive  evidence  of  syphilis 
with  a  formula  like  that  of  tabes. 

Syringomyelia  is  distinguished  by  the  presence  of  peculiar  sensor}- 
and  trophic  disorders. 

Neuritis  caused  by  lead  poisoning  is  detected  by  the  history  of  the 
case,  its  tendency  to  affect  the  extensors  of  the  arm  chiefly,  and  the 
absence  of  a  progressive  tendency.  Sometimes,  however,  lead  poisoning 
and  palsy  end  in  a  progressive  muscular  atrophy. 

Ordinar}^  multiple  neuritis  is  distinguished  easily  by  its  rapid  onset 
and  the  presence  of  sensory  symptoms. 

The  hereditary  or  neuritic  type  of  progressive  muscular  atrophy  is 
characterized  by  its  attacking  first  and  mainh^  the  legs  and  forearms, 
by  the  presence  of  a  good  deal  of  sensory  disturbance,  of  typical  degenera- 
tion reactions,  and  of  a  hereditary  or  familj^  history. 

Treatment. — The  patient  should  be  well  fed  and  have  rest,  quiet 
and  fresh  air.  Careful  local  faradization  and  galvanization  of  the  spine 
and  affected  parts  are  indicated.  Massage  does  no  good,  but  very  care- 
fully applied  active  and  passive  exercises  are  useful. 

Hypodermatic  injections  of  strychnine  in  the  affected  member,  gr.  3^^o 
to  3'^o  daily,  the  internal  use  of  arsenic,  phosphorus,  iron,  quinine  and 
cod-liver  oil  sometimes  are  beneficial. 

In  cases  with  a  syphilitic  history,  specific  measures  are  indicated  and 
injections  of  salvarsan  should  be  given  to  the  toxic  limit. 

It  is  necessarj^  to  admit  that  we  have  no  remedy  for  non-luetic  types 
of  this  disease. 

THE  LUETIC  TYPE  OF  SPINAL  ATROPHY 

{Remittent  Type  of  Chronic  Anterior  Poliomyelitis) 

This  form  of  atrophy  runs  a  course  like  that  of  a  chronic  anterior 
poliomyelitis  and  it  is  described  under  the  head  of  myelitis,  p.  243. 


298  DISEASES    OF    THE    NERVOUS    SYSTEM 

HEREDITARY  TYPES  OF  SPINAL  AND  NEURO -SPINAL  ATROPHY 

These  are:  (1)  the  infantile  form  (Werding-Hoffman),  (2)  the  adult 
form  (described  by  the  author),  (3)  the  Charcot-Marie-Tooth  type. 

1.  In  the  infantile  form  the  disease  begins  in  the  first  or  second 
years  of  life.  It  attacks  first  the  muscles  of  the  pelvic  girdle,  the  back, 
buttocks,  hips.  It  then  goes  to  the  shoulders  and  neck  muscles  and  finally 
involves  the  forearms,  legs,  hands  and  feet.  The  atrophy  is  symmetrical 
and  at  first  is  concealed  by  subcutaneous  fat.  Paralysis  and  atrophy 
go  along  together.  There  are  no  fibrillary  twitchings.  The  paralysis 
is  flaccid  and  the  deep  reflexes  disappear.  Scoliosis  and  leg  deformities 
occur.     There  are  no  sensory  symptoms. 

2.  The  adult  form,  familial  type  of  progressive  spinal  atrophy,  attacks 
the  patient  in  the  third  or  fourth  decade  of  life.  It  begins  in  the  thighs 
or  arms  but  soon  extends  to  the  legs  and  forearms.  The  paralysis  seems 
to  precede  the  atrophy.  There  are  some  fibrillary  twitchings,  and 
degenerative  electrical  reactions  are  present.  The  paralysis  is  flaccid, 
deep  reflexes  disappear.  The  disease  runs  a  relatively  rapid  course. 
In  six  months  the  patient  is  unable  to  walk;  the  arms  are  affected  and 
later  the  bulbar  muscles.     The  patient  dies  within  a  year. 

No  exciting  cause  is  known.  The  serological  formula  is  negative, 
so  that  the  disease  is  not  a  manifestation  of  syphilis. 

HEREDITARY  MUSCULAR  ATROPHY  OF  PERONEAL  TYPE 

{Charcot-Marie-Tooth  Type) 

This  is  a  hereditary  or  family  muscular  atrophy  of  central  Cand 
neuritic)  origin,  attacking  the  legs  and  later  the  forearms.  The  symp- 
tomatology of  the  disease  has  had  so  many  accessions  that  its  clinical 
features  are  much  obscured.  I  follow  the  descriptions  of  Marie  and 
Leri,  and  my  own  personal  observation  of  several  cases. 

The  disease  is  quite  rare.  It  affects  males  more  than  females,  but  the 
difference  is  not  great.  It  almost  always  begins  before  the  age  of  twenty. 
It  attacks  first  usually,  the  muscles  of  the  leg,  not  the  foot,  involving  the 
peronei,  causing  a  varo-equinus  or  a  flail  foot;  then  calf  muscles,  the  ex- 
tensors of  the  toes  and  the  intrinsic  muscles  of  the  foot  are  involved. 
The  thighs  escape  till  later.  After  some  time  the  forearms  and  small 
hand  muscles  are  reached,  The  shoulders  and  arm,  neck  and  trunk 
muscles  escape.  There  are  occasionally  fibrillary  contractions,  and  al- 
ways partial  or  complete  degenerative  electrical  reactions.  The  patients 
complain  of  some  pain  and  numbness,  but  there  is  no  anaesthesia. 

The  characteristic,  then,  of  this  form  of  atrophy  is  that  it  affects  the 
legs,  rarely  going  above  the  knee,  and  producing  a  rather  symmetrical 


MUSCULAR   ATROPHIES    AND    DYSTROPHIES 


299 


atrophy  of  these  limbs,  so  that  in  the  later  stages  the  legs  look  very 
spinclle-like,  and  there  is  no  pseudo-hypertrophy  at  any  period  in  the 
progress.  In  some  cases  the  hands  and  forearms  are  attacked  in  a  similar 
way,  producing  a  symmetrical  and  progressive  atrophy  of  the  parts. 
Gowers  has  observed  a  case  in  which  with  the  characteristic  involve- 
ment of  the  forearms  there  was  also  an  involvement  of  the  face,  in  a 
fashion  somewhat  similar  to  that  seen  in  the  facio-scapulo-humeral  type 
of  dystrophy. 

The  disease  runs  a  long  course,  with  remissions,  and  resembles  in 
prognosis  the  dystrophies. 

Some  authorities  assert  that 
the  disease  is  due  to  a  progres- 
sive degenerative  neuritis.  In  the 
writer's  opinion,  the  anterior  horns 
of  the  spinal  cord  are  primarily 
attacked,  a  view  recently  con- 
firmed by  Marinesco.  It  is  there- 
fore a  disease  of  the  peripheral 
motor  neurons. 

The  treatment  is  the  same  as 
for  the  other  forms  of  hereditary 
m-uscular  atrophy. 

A  disease  apparently  related 
to  the  above  is  progressive  hyper- 
trophic interstitial  neuritis  (De- 
jerine  and  Sottas).  This  also  af- 
fects first  and  mainly  the  legs 
and  feet  and  runs  a  course  like 
that  of  the  Charcot-Marie  disease. 
It  is  characterized  by  progressive 
atrophy,  by  a  palpable  hyper- 
trophy of  the  nerves,  kypho-sco- 
liosis  and  bulbar  symptoms.  It 
is  usually  of  hereditary  and  familial  origin  and  begins  injnfancy  or 
adolescence. 

GLOSSO-LABIO-LARYNGEAL  PARALYSIS 

(Progressive  Bulbar  Paralysis) 

This  is  a  disease  characterized  by  progressive  wasting  and  paralysis 
of  the  muscles  of  the  tongue,  lips,  palate  and  throat,  due  to  an  atrophy 
of  the  nuclei  of  the  nerves  supplying  those  parts. 

Etiology. — It  is  a  disease  of  the  degenerative  period  of  life,  most 
cases  occurring  after  forty  and  between  that  time  and  seventy. 


Fig.    136.- 


-P^eroneal    type   of   atrophy. 
{Marie.) 


300  DISEASES    OF    THE    NEEVOUS    SYSTEM 

The  disease  begins  later  in  life  than  spinal  atrophy.  It  occurs 
rather  oftener  in  men  than  women.  A  neurotic  heredity  is  some- 
times noted.  Exposure  to  cold  and  excessive  use  of  the  muscles  in 
talking,  mental  strain,  debilitating  influences,  lead  and  syphilis  are  causal 
factors. 

The  element  of  syphilis  in  producing  this  type  of  atrophy  has  been 
studied  by  the  writer,  and  he  has  found  that  in  over  20  per  cent,  there  is 
a  history  of  infection.  It  has  occurred  in  two  cases  as  a  terminal  sjanp- 
tom  in  locomotor  ataxia.  Dr.  Janeway  tells  me  of  a  case  in  which  there 
was  a  prompt  remission  by  the  use  of  salvarsan. 

Symptoms. — The  tongue  is  the  part  first  affected,  and  the  patient 
finds  that  he  speaks  indistinctly  and  cannot  especially  articulate  the 
lingual  consonants  I,  r,  n  and  t.  The  tongue  movements  become  weak. 
It  cannot  be  elevated  and  is  protruded  only  a  little  distance.  It  gradually 
atrophies  and  looks  scarred  and  wrinkled.  The  lips  become  weak  and 
the  patient  cannot  whistle  nor  make  the  consonants  p,  5,  m,  or  the 
vowel  0.  The  saliva  begins  to  dribble  from  the  mouth.  Disturbance 
in  swallowing  soon  develops.  Hard  solids  are  taken  with  difficult}^, 
next  fluids,  while  semisolids  are  generally  managed  best.  The  lips 
finally  become  so  paralyzed  that  the  mouth  cannot  be  shut,  and  the  lower 
part  of  the  face  is  motionless  and  expressionless.  The  upper  face  wears 
an  expression  of  anxiety  and  suffering,  the  saliva  dribbles  constantlj^ 
and  the  whole  physiognomy  of  the  patient  becomes  characteristic  and 
pitiful  in  the  extreme.  The  facial  nerve  may  get  somewhat  involved. 
Articulation  becomes  almost  entirely  lost;  the  voice  has  a  nasal  twang 
from  paralysis  of  the  palate. 

The  patient  has  tired  and  uncomfortable  sensations  of  dryness 
and  stiffness  about  the  throat.  There  is  no  pain  or  anaesthesia,  but 
occasionally  there  is  impairment  of  the  sense  of  taste.  The  throat 
reflex  is  usually  lost,  so  that  tickling  it  causes  no  reaction. 

Electric  irritability  is  at  first  unchanged,  but  in  the  later  stages 
partial  degeneration  reaction  occurs.  In  rare  cases  there  is  a  rapid 
pulse  and  still  more  rarely  glycosuria. 

The  laryngeal  reflex  becomes  weak;  the  adductor  muscles  act  feebly 
also,  but  abductor  paralysis  is  rare. 

The  mind  is  not  affected,  but  there  are  often  an  emotional  weakness 
and  tendency  to  tears — not  at  all  unreasonable  in  view  of  the  distressing 
nature  of  the  malady. 

The  disease  is  often  the  terminal  stage  of  spinal  muscular  atrophy; 
it  may  be  associated  with  the  latter,  with  amyotrophic  lateral  sclerosis, 
or  with  ophthalmoplegia.     All  these  types  may  occur  together. 

It  runs  a  progressive  course,  with  remissions  of  a  few  weeks  or  months. 
It  lasts  from  two  to  three  or  four  j^ears. 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES 


301 


The  termination  is  eventually  fatal  except  perhaps  in  luetic  cases. 
Death  occurs  through  interference  with  swallowing,  and  inanition  or  a 
broncho-pneumonia  or  Ijronchitis  may  develop  which  ends  the  patient's 
life. 

Pathology. — The  primary  lesion  is  found  in  the  nuclei  of  origin  of 
the  hypoglossal,  glossopharyngeal,  vagus  and  spinal  accessory  nerves. 
The  raphe  fibres  and  the  anterior  pyramids  are  also  usually  somewhat 
involved.  There  is  sometimes  atrophy  of  the  cells  of  the  facial  nerve 
and  of  the  nucleus  ambiguus,  which  is  the  motor  nucleus  of  the  vagus. 
The  brunt  of  the  disease  falls,  therefore,  upon  those  more  superficial 


Fig.  137. — Bulbar  palsy;  nucleus  of  hypoglossal.  The  dark  cells  are  nearlj^ 
obliterated  with  pigment,  X2-3.  To  the  right  are  four  cells  in  different  stages  of 
degeneration,  X 1-6. 


or  posterior  nuclei  which  are  representative  of  a  continuation  of  the 
anterior  cornual  cells.  If  the  disease  is  complicated  with  amyotrophic 
lateral  sclerosis,  or  progressive  muscular  atrophy,  or  ophthalmoplegia, 
we  find  atrophy  in  the  pyramidal  tracts,  cord  and  ocular  nuclei.  The 
atrophic  process  is  similar  to  that  observed  in  the  spinal  disease. 

The  muscles  of  the  tongue,  and  to  a  less  extent  the  orbicularis  oris 
and  the  throat  muscles,  show  evidences  of  degeneration  and  atrophy. 
In  some  cases  the  tongue  is  not  shrivelled,  owing  to  the  presence  of 
a  fatty  deposit,  and  on  account  of  this  the  disease  has  been  divided 
into  atrophic  and  paralytic  types,  but  this  distinction  is  unnecessary. 


302  DISEASES    OF    THE    NERVOUS    SYSTEM 

Diagnosis. — -The  disease  must  be  distinguished  from  polioenceph- 
alitis inferior,  bulbar  apoplexy,  tumors,  and  softening,  from  multiple 
sclerosis,  and  from  chronic  lesions  of  the  cerebral  hemispheres  caus- 
ing pseudo-bulbar  paralysis.  It  must  also  be  distinguished  from 
myasthenic  bulbar  palsy.  The  slow  onset,  the  progressive  course,  the 
bilateral  character,  the  absence  of  involvement  of  sensory  nerves,  and 
the  degenerative  reactions  are  sufficient  for  a  diagnosis.  In  myasthenic 
bulbar  palsy  there  is  progressive  paralysis,  but  none  of  the  typical  atrophy 
of  the  parts;  the  ocular  muscles  are  usually  involved;  often  these  patients 
get  well.  It  is  important  always  to  note  whether  there  are  ophthal- 
moplegia and  spinal  muscular  atrophy  associated  with  the  disease. 

Treatment. — ^The  patient  should  be  kept  quiet,  and  he  should  be  over- 
fed. The  same  drug  treatment  as  in  the  spinal  disease  is  indicated. 
Small  doses  of  morphine,  gr.  3^4  to  ^^q,  and  of  atropin  may  be  given  also. 
It  is  important  in  these  cases,  where  there  is  any  suspicion  of  syphilis, 
to  give  salvarsan  and  a  course  of  hypodermatic  injections  of  mercury. 
Massage  to  the  neck  and  face  gives  temporary  relief.  Careful  voluntary 
exercises  of  the  weak  parts  are  helpful.  Electricity  should  be  tried 
for  a  short  time  twice  or  even  thrice  daily,  if  possible.  The  faradic 
current  may  be  used,  alternating  or  combined  with  the  galvanic.  Gal- 
vanization of  the  neck  and  medulla  does  no  good.  After  a  time  it  may 
be  necessary  to  feed  with  a  tube  or  even  to  do  tracheotomy. 

INFANTILE  HEREDITARY  BULBAR  PALSY 

There  have  been  reported  cases  of  progressive  bulbar  palsy  beginning 
in  infancy  and  of  hereditary  or  family  type.  They  are  often  associated 
with  spinal  atrophy  and  amyotrophic  lateral  sclerosis.  Some  of  these 
cases  are  probably  muscular  dystrophies. 

MYASTHENIA  GRAVIS 

(Asthenic  Bulbar  Paralysis  and  Asthenic  Bulbospinal  Paralysis) 

These  names  are  given  to  a  chronic  frequently  remitting  disorder 
characterized  by  the  symptoms  of  mesencephalic  and  bulbar  paralysis  or 
by  the  symptoms  of  this  condition  and  of  progressive  spinal  paralysis, 
the  distinguishing  features  being  that  there  is  no  muscular  atrophy, 
that  the  cases  often  continue  on  for  many  years  instead  of  going  on  to  a 
fatal  issue,  and  also  by  the  fact  that  on  autopsy  no  surely  characteristic 
microscopical  changes  are  found. 

Etiology. — Little  is  known  as  to  the  cause  of  the  disease.  The 
majority  of  cases  have  been  under  the  age  of  thirty,  but  a  patient  of 
my  own  was  over   fifty  years  of  age  and  another  over  forty.     It  is  some- 


MUSCULAR  ATROPHIES  AND  DYSTROPHIES 


303 


times  associated  with  anaemia  and  also  with  intestinal  toxsemia.  Re- 
cently it  has  been  found  that  there  are  lymphoid  deposits  in  the  mus- 
cles, and  in  some  cases  the  thymus  is  present  and  diseased.  Those  causes 
which  are  found  in  progressive  bulbar  and  spinal  paralysis,  viz.,  overwork, 
mental  strain,  are  sometimes  found  here. 

Symptoms. — -The  disease  usually  begins  gradually  and  oftenest 
affects  first  the  muscles  of  the  throat  and  face  and  of  the  eyes.  The 
patient  notices  a  general  feeling  of  unnatural  weakness,  and  gets 
more  easily  tired  at  his  work.  Then  he  finds  that  sometimes  he  sees 
double,  or  one  of  his  lids  droops  and  it  is  difficult  to  keep  the  eye  open; 
then  he  has  to  give  up  chewing  solid  food  because  it  tires  the  jaws.  Speech 
soon  tires  him;  the  voice  may  be  nasal;  and  he  has  to  swallow  with  some 


Fig.  138. — Lymphorrhage  in  muscle  in  myasthenia.     {Dr.  F.  S.  Mandlebaum.) 


care.  The  arms  get  easily  weak  and  they  tire  at  their  accustomed  tasks. 
Digestion  is  slow  and  constipation  may  occur.  The  abdominal  muscles 
relax  and  the  abdomen  is  distended. 

The  mental  and  other  bodily  functions  are  little  disturbed.  There  is 
little  or  no  pain,  no  emaciation  or  local  atrophy;  no  spasm  or  twitching. 
On  stimulating  the  muscles  with  an  electric  current  the  responses  get 
weaker  and  finally  cease.  After  a  rest  they  return  (myasthenic,  elec- 
trical reaction) .  The  same  phenomenon  occurs  on  tapping  the  tendons 
of  affected  muscles.  The  symptoms  are  characterized  by  remissions; 
after  a  patient  has  reached  a  point  at  which  he  is  almost  moribund,  he 
begins  to  get  stronger  again  and  may  slowly  get  into  a  state  of  compara- 
tive strength;  then  the  symptoms  slowly  return.  In  this  way  the  disease 
may  continue  for  a  number  of  years.  The  patient  sometimes  dies  of  ex- 
haustion, but  he  often  recovers  if  properly  treated. 


304  DISEASES    OF    THE    NERVOUS    SYSTEM 

Pathological  Anatomy, — In  the  half-dozen  early  autopsies  no  lesion 
of  the  nervous  system  was  found,  except  microscopical  changes  in  the  cell 
of  the  motor  nuclei.  Later  lymphoid-cellular  deposits  (lymphorrhages) 
in  the  muscles  and  a  persistent  or  diseased  thymus  have  been  found. 
Most  careful  examinations  of  the  blood,  urine,  gastric  and  intestinal 
contents  have  been  made  for  me  by  Dr.  T.  W.  Hastings  but  have  failed 
to  throw  light  on  the  disease,  which  is  due,  probably,  to  a  toxaemia  of 
intestinal  or  blood-gland  origin. 

Diagnosis. — ^The  clinical  characteristics  which  distinguish  this  disease 
from  progressive  muscular  atrophy  and  true  bulbar  palsy  are  the  transient 
diplopia  and  ptosis,  the  absence  of  any  true  atrophy  of  the  muscles  of 
the  face  or  tongue  or  extremities,  the  absence  of  fibrillary  twitchings, 
the  presence  of  the  myasthenic  reaction  and  the  irregular  course  with 
remissions.  Like  these  other  diseases,  however,  asthenic  paralysis  is 
not  accompanied  by  any  disturbance  of  sensibility  or  any  impairment 
of  the  sphincters. 

The  treatment  consists  in  complete  rest,  careful  attention  to  feeding, 
and  the  use  of  iron,  arsenic,  strychnia,  the  calcium  salts  and  intestinal 
disinfectants.  In  some  cases  excellent  results  are  obtained  by  injections 
of  massive  doses  of  strychnia,  up  to  gr.  Ya.  ter  die  hypodermically.  By  one 
or  other  of  these  measures  all  patients  if  seen  reasonably  early  can  be 
relieved  or  cured. 

AMYOTROPHIC   LATERAL  SCLEROSIS 

(Spastic  Form  of  Progressive  Muscular  Atrophy) 

This  disease  is  one  which  has  the  closest  possible  kinship  to  progressive 
muscular  atrophy.  Its  clinical  symptoms,  however,  are  somewhat  dif- 
ferent, and  anatomically  there  is  a  somewhat  more  extensive  and  peculiar 
change.  Amyotrophic  lateral  sclerosis,  or  Charcot's  disease,  is  char- 
acterized by  progressive  spasticity  with  atrophy,  rigidity  and  contrac- 
tures of  the  limbs,  ending  or  beginning  often  with  bulbar  symptoms. 

Etiology. — It  is  a  rarer  disease  than  progressive  muscular  atrophy, 
and  occurs  most  often  between  the  ages  of  thirty  and  fifty,  involving 
the  second  part  of  adult  life.  Rare  cases,  however,  have  been  reported 
as  occurring  in  childhood.  The  female  sex  is  rather  more  often  affected. 
No  definite  exciting  cause  is  known.  It  is  sometimes  due  to  syphilis. 
It  is,  probably,  fundamentally  a  disease  of  involution;  i.e.,  a  teratological 
defect,  the  first  and  second  motor  neurons  degenerating  because  of 
inherently  deficient  vitality.  This  state  of  affairs,  however,  underlies 
the  other  spinal  myopathies  also. 

Symptoms. — Spinal  Onset. — In  its  spinal  and  more  common  form  there 
is  first  noticed  a  weakness  and  clumsiness  of  one  hand  and  this  may  be 
associated  with  some  subjective  sensation  like  a  numbness.     No  atrophy 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES  305 

is  seen  but  some  twitchings  of  the  muscles,  and  irregular  jerky  tremor  of 
the  fingers  and  hand  occur.  Soon  the  other  hand  and  then  the  legs  are 
involved,  so  that  in  a  few  months  walking  tires  the  patient,  going  up- 
stairs is  cUfiicult,  the  feet  tend  to  drop  because  the  anterior  tibials  are 
weak.  Cramps  are  noticed  in  the  leg  muscles,  and  the  same  paraes- 
thesise  are  felt  as  in  the  hands  and  arms.  In  less  acute  cases  the  lower 
limbs  are  net  involved  for  a  long  time;  i.e.,  for  one  or  two  years.  Ex- 
amination after  the  disease  has  developed  shows  some  slight  atrophy  of 
the  intrinsic  hand  muscles  and  perhaps  of  the  forearms.  The  fibrillary 
twitchings  are  present  and  sometimes  are  extremely  marked  affecting 
the  shoulder  and  trunk  muscles  as  well  as  the  arms.  The  reflexes  are 
much  exaggerated,  especially  those  of  the  lower  extremities;  there  is 
ankle  clonus  and  the  dorsal  flexion  of  the  great  toe  (Babinski's  sign)  is 
present.     The  wrist,  elbow  and  perhaps  the  jaw-jerk  are  also  very  active. 

The  disease  usually  progresses  steadily,  until  the  upper  extremities 
become  almost  useless  and  the  lower  extremities  nearly  as  much  so. 
Atrophy  has  now  set  in,  of  the  same  type  as  that  of  progressive  muscular 
atrophy.  No  special  sensory  symptoms  except  sense  of  weariness  and 
aching  are  to  be  noted  and  there  is  no  involvement  of  the  sphincters. 
Finally,  in  about  one  and  one-half  to  two  years  the  medulla  becomes 
affected,  and  there  is  weakness,  stiffness,  cramp  and  atrophy  of  the 
tongue;  the  lips  are  less  mobile  and  speech  and  swallowing  are  affected, 
the  symptoms  being  the  same  as  in  bulbar  palsy  except  that  there  is 
evidence  of  a  rigidity  and  a  tendency  to  cramp  and  contracture,  while 
the  atrophy  comes  later. 

Bulbar  Onset. — Sometimes  the  disease  begins  in  the  medulla.  There 
is  then,  on  the  whole,  a  more  rapid  progress,  a  later  atrophy  and  a  slighter 
tendency  to  remission  than  in  the  other  myelopathic  atrophies.  The 
patient  first  notices  some  difficulty  in  speaking  or  swallowing.  He  feels 
at  times  a  spasmodic  drawing  of  the  tongue  or  stiffness  of  the  cheek  or 
lips.  Soon  after  there  appear  a  weakness  and  stiffness  of  the  legs  and 
arms.  The  symptoms  progress  rather  slowly.  The  speech  becomes  dis- 
turbed; swallowing  is  difficult;  the  arms  atrophy  and  become  stiff  and 
rigid,  producing  characteristic  deformities.  There  is  great  exaggeration 
of  the  reflexes;  the  legs  show  the  presence  of  ankle  clonus;  all  the  arm 
reflexes  are  increased,  and  the  jaw  is  stiff  and  has  a  very  lively  jerk  when 
struck.  The  patient  suffers  little  from  pain.  There  are  no  anaesthesias 
and  no  sphincter  trouble,  except  in  the  last  stages  of  the  disease. 

Pathological  Anatomy. — Post-mortem  examinations  show  a  very 
marked  sclerosis  involving  the  direct  and  crossed  pyramidal  tracts;  also 
some  of  the  short -fibre  systems  of  the  lateral  column.  The  anterior 
cornual  cells  are  atrophied,  as  in  progressive  muscular  atrophy.  Lesions 
are  also  seen  at  times  in  the  columns  of  Goll.     In  fact,  the  post-mortem 

20 


306 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


findings  resemble  entirely  those  of  progressive  muscular  atrophy,  except 
that  there  is  a  sharper  accentuation  of  the  disease  in  the  lateral  tracts. 
In  the  medulla  the  nuclei  of  the  hypoglossal  and  other  motor  cranial 
nerves  will  be  found  diseased  and  the  pyramidal  tracts  also.  The  lesion 
of  the  white  columns  diminishes  in  intensity  from  below  up,  so  that  as 
one  gets  into  the  cerebral  peduncles  very  little  if  any  is  to  be  seen.  In 
a  few  cases,  however,  the  process  has  been  traced  to  the  motor  cortex  and 
changes  even  in  that  part  have  been  discovered.  In  a  case  of  my  own, 
which  was  very  closely  studied  and  reported  upon  by  Dr.  Joseph  Collins, 
the  sclerosis  of  the  motor  tracts  did  not  reach  above  the  medulla,  and 
there  was  no  lesion  of  any  moment  in  the  cortical  motor  cells. 

In  amyotrophic  lateral  sclerosis  the   degenerative   process   attacks 
first   the   terminal   fibres   and    collaterals   of   the   cortico-spinal   motor 


Fig.  139. — Amyotrophic  lateral  sclerosis.     Shrunken  anterior  horns,  lateral  sclerosis. 


neurons.  The  next  part  attacked  is  the  anterior  cornual  cell.  We 
have,  therefore,  the  curious  and  perplexing  phenomenon  of  a  disease 
which  attacks  the  cell  body  of  one  neuron  and  the  terminal  neuraxon 
of  another  neuron  just  above  it.  It  is  difficult  to  explain  this  upon 
the  ordinary  lines  of  nerve-cell  pathology.  Still,  we  have  analogies, 
perhaps,  both  in  locomotor  ataxia  and  in  multiple  neuritis. 

The  diagnosis  of  amyotrophic  lateral  sclerosis  must  be  made  from 
transverse  myelitis,  multiple  sclerosis,  and  the  other  forms  of  progress- 
ive muscular  atrophy.  The  diagnosis  is  based  upon  the  very  striking 
and  progressive  atrophy  associated  with  myokymia,  exaggerated  reflexes, 
rigidity  and  contractures,  without  any  sensory  symptoms  or  sphincter 
troubles.  The  diagnosis  from  ordinary  bulbar  palsy  depends  upon 
the  appearance  of  stiffness,  cramps,  exaggerated  reflexes  and  rigidity 
displayed    in  the  muscular  supply  of    the  facial,   the  trigeminal   and 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES  307 

the  glossopharyngeal,  and  the  tenth,  eleventh  and  twelfth  cranial 
nerves. 

The  prognosis  is  invariably  bad,  but  in  those  types  beginning  in 
the  legs  and  arms  life  may  be  prolonged  a  number  of  years. 

The  treatment  is  the  same  as  that  for  progressive  muscular  atrophy. 

THE  PROGRESSIVE  MUSCULAR  DYSTROPHIES 

As  I  have  already  stated,  there  are  various  forms  of  progressive 
muscular  atrophy  to  which  the  special  name  of  "dystrophy"  is  given, 
because  they  are  hereditary  in  character  and  because  the  muscular  end 
of  the  motor  neuron  is  apparently  the  first  and  the  most  severely  at- 
tacked. Recent  and  closer  study  of  the  pathology  of  muscular  dystrophy 
tends  to  show  that  the  lesion  is  not  in  the  muscle  and  terminal  of  the 
motor  nerves  alone,  but  that  the  peripheral  motor  neuron  is  also  to 
some  extent  affected.  The  clinical  characteristics  of  the  muscular 
dystrophies,  however,  are  pretty  distinct  and  are  sufficient  to  justify 
the  separation  of  them  into  a  different  class. 

The  general  characteristics  of  the  dystrophies  as  distinguished  from 
the  spinal  atrophies  are  the  following: 

1.  There  is  generally  a  hereditary  or  family  history. 

2.  They  begin  rather  early  in  life. 

3.  The  progress  is  very  slow  with  sometimes  long  remissions. 

4.  The  limbs  are  affected  symmetrically,  i.e.,  both  shoulders  or 
both  legs  at  about  the  same  time. 

5.  The  tendency  is  for  the  disease  to  attack  the  root  or  proximal 
segments  of  the  extremities  of  the  body,  i.e.,  the  hips  and  the  pelvic 
girdle  or  the  arms  and  the  shouldei -girdle  first,  and  later  the  peripheral 
segments  of  the  limbs. 

6.  There  occurs  occasionally  pseudo-muscular  hypertrophy  of  some 
muscles. 

7.  There  is  occasionally  along  with  the  atrophy  myotonus  of  some 
muscles. 

8.  There  is  no  idio-muscular  reaction. 

9.  There  are  no  fibrillary  twitchings. 

10.  The  deep  reflexes  disappear  pari  passu  with  the  atrophy  of  the 
muscles. 

11.  The  electrical  reactions  show  no  degeneration  change  until  very 
late. 

12.  There  occur  certain  fibro-muscular  contractures  causing  deformities 
of  the  body. 

A  number  of  types  have  been  described,  the  distinctions  being  based 
chiefly  on  the  part  of  the  body  first  affected.     These  types  are  not  of 


308 


DISEASES    OF    THE    NERVOUS    SYSTEM 


great   importance,    but   may   be    enumerated    here    for    convenience. 
(Fig.  140): 

1.  Pseudo-muscular  hypertrophy.     Allied  to  it  is: 

(a)  Leyden-Mobius  or  hereditary  type,  appearing  in  children, 
beginning  in  the  back  and  pelvic  girdle  and  lower  limbs.  The  congenital 
type  of  Hoffman  is  also  allied  to  this. 

2.  Erb-s  juvenile  type,  or  scapulo-humeral  type,  beginning  in 
childhood  or  youth,  usually  in  the  shoulder-girdle  and  trunk. 


A.  B. 

Fig.  140. — Showing  the  parts  first  attaclied  in  the  different  types  of  muscular  dys- 
trophy and  muscular  atrophy.  The  shaded  parts  in  A  show  the  place  of  onset  of  pro- 
gressive muscular  atrophy  of  ordinary  or  Duchenne-Aran  type,  and  of  types  2  and  3  in 
text.     B  shows  place  of  onset  of  types  1  and  (a)  in  text. 

3,  Landouzy-Dejerine  type,  or  infantile  progressive  muscular  atrophy 
of  Duchenne,  or  facio-scapulo-humeral  type.  It  resembles  the  preceding 
form,  with  the  exception  that  it  involves  also  the  face. 

The  peroneal  or  leg  type  has  been  classed  with  the  dystrophies, 
but  is  probably  of  myelo-neural  origin,  and  has  been  described  with  the 
spinal  atrophies  (see  page  296). 

The  essential  unity  of  all  these  different  forms  is  shown  by  the  fact 
that  cases  occur  in  which  pseudo-hypertrophy  takes  place  in  the  scapulo- 
humeral and  other  types,  by  the  fact  that  a  disease  resembling  pseudo- 


MUSCULAR   ATROPHIES    AND    DYSTROPHIES  309 

hypertrophic  paralysis  occurs  without  any  hypertrophy,  and  by  the 
fact  that  different  types  occur  in  the  same  family. 

The  dystrophies  are,  in  a  considerable  proportion,  of  hereditarj^ 
origin  or,  at  least,  run  in  families.  Among  twenty-nine  cases  observed 
by  myself,  there  was  a  distinct  family  history  in  12  per  cent.  They 
affect  boys  much  oftener  than  girls,  in  the  proportion  of  about  one  to 
five.  In  my  own  cases,  there  were  twenty-four  males  and  five  females. 
The  great  majority  occur  under  the  age  of  twenty,  and  a  majority 
under  the  age  of  ten  years.  Thus,  among  my  cases,  there  were  under 
five  years,  eleven;  under  ten  years,  seventeen;  and  under  twenty  years, 
there  were  twenty-two.  They  may  develop,  however,  as  late  as  the 
fortieth  year. 

The  so-called  '^peroneal  type"  develops,  on  the  whole,  rather  late, 
while  pseudo-muscular  hypertrophy  and  the  allied  hereditary  types 
begin  very  early,  often  in  infancy,  and  some  children  have  even  never 
known  what  it  was  to  walk. 

1  he  distribution  of  the  types  probably  differs  somewhat  in  different 
countries  and  races.  In  this  country,  in  the  Montefiore  Home,  where 
the  patients  are  mainly  Hebrews,  the  pseudo-muscular  hypertrophy 
and  the  hereditary  type  of  Leyden-Mobius  is,  by  all  odds,  the  most 
common.  In  the  personal  cases,  seen  by  myself,  both  in  private  practice 
and  in  my  clinic,  pseudo-muscular  hypertrophy  is  also  most  frequent. 
The  shoulder-arm  type  of  Erb  comes  next  in  frequency,  while  the  facio- 
scapulo-humeral  type  is  extremely  rare,  there  being  only  one  in  thirty 
cases.  The  peroneal  type  is  not  common.  Among  the  native  Americans 
the  dystrophies  often  develop  later  in  life,  take  a  longer  and  less  serious 
course,  and  sometimes  become  arrested.  In  fact,  the  common  type 
among  the  native  classes,  which  I  have  seen,  is  one  in  which  the  pelvic 
girdle,  back  and  shoulder  girdle  become  gradually  affected  rather  sym- 
metrically, so  that  the  patient  becomes  greatly  wasted,  but  is  still  able 
to  walk  and  use  the  forearms,  the  face  and  throat  not  being  affected. 
These  cases  form  the  living  skeletons  of  the  museums.  This  form  of 
dystrophy  begins  usually  below  and  ascends,  being  first  a  hip-girdle  and 
trunk  affection,  then  a  shoulder-girdle  affection,  and  is,  therefore,  a  sort 
of  combination  of  the  hereditary  (Leyden-Mobius)  and  of  the  so-called 
juvenile  type  (Erb). 

All  the  cases  which  have  come  under  my  observation  in  New  York 
could  be  grouped,  then,  in  the  following  way: 

1.  The  typical  cases  of  pseudo-muscular  hypertrophy,  beginning 
in  the  leg,  but  soon  involving  the  hip-girdle  and  shoulder. 

2.  The  root  type,  beginning  in  the  hips  usually  and  back  muscles, 
and  extending  to  the  shoulder  and  trunk  muscles,  not  necessarily  ex- 


310 


DISEASES    OF    THE    NERVOUS    SYSTEM 


tending  to  the  legs  and  arms,  at  least,  not  until  very  late  in  the  disease, 
and  accompanied  often  with  some  pseudo-hypertrophy. 

3.  The  peroneal  type  which,  in  its  pure  form,  is  extremely  rare,  but 
of  which  irregular  types  are  not  so  uncommon. 

4.  The  facio-scapulo-humeral  type,  which  is  the  rarest  of  all. 
Among  my  cases  there  were  of  the  first  type,  eleven;  of  the  second 

type,  twelve;  of  the  third  type,  four; 
and  of  the  fifth  type,  one. 

PSEUDO -MUSCULAR  HYPERTROPHY 

{Atrophia  Musculorum  Lipomatosa) 

This  is  a  disease  beginning  in  child- 
hood and  characterized  by  a  symmet- 
rical, progressive  atrophy  of  muscles, 
associated  with  an  apparent  muscular 
hypertrophy  due  to  a  deposit  of  fat  in 
the  wasting  muscles. 

Etiology. — The  disease  attacks  boys 
much  oftener  than  girls.  It  begins,  in 
the  vast  majority  of  cases,  under  the 
age  of  ten,  often  at  the  close  of  in- 
fancy, very  rarely  not  till  after  pu- 
berty. Heredity  is  a  very  important 
factor  (in  three-fifths  of  the  cases),  the 
hereditary  influence  being  almost  al- 
ways transmitted  by  the  mother.  A 
psychopathic  or  neuropathic  condition 
is  often  found  in  the  ancestry.  Syph- 
ilis, intemperance,  consanguinity,  are 
not  factors  in  hereditary"  causation. 
Injury  and  an  acute  disease  sometimes 
appear  to  act  as  exciting  causes. 
Symptoms. — The  first  symptom  noticed  is  a  weakness  in  the  legs, 
which  shows  itself  in  a  peculiar  "waddling  gait"  and  a  tendency  to 
stumble  and  fall.  A  little  later  (fifth  or  sixth  year)  an  apparent  hyper- 
trophy of  the  leg  muscles,  particularly  of  those  of  the  calves,  develops. 
The  extensors  of  the  knee  or  one  of  them  and  the  gluteal  and  lumbar 
muscles  may  also  be  affected.  Sometimes  the  hypertrophy  is  very  great, 
at  other  times  it  is  barely  noticeable.  The  affected  part  has  a  peculiar, 
hard,  non-elastic  feeling  to  the  hand,  not  like  that  of  normal  muscle. 
In  the  upper  part  of  the  body  the  hypertrophy  oftenest  attacks  the  infra- 
spinatus, the  supraspinatus  and  the  deltoid  (Fig.  141).     The  lower  parts  of 


Fig 


141 . — Pseudo-muscular 
trophy. 


hyper- 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES 


311 


the  pectoralis  major  and  latissimus  dor.si  are  also  usually  atrophied, 
giving  a  characteristic  appearance  to  the  shoulders.  The  upper-arm 
muscles  usually  become  wasted,  the  forearm,  neck,  and  face  rarely. 
The  tongue  may  be  hypertrophied. 

Along  with  the  pseudo-hypertrophy  there  occurs  an  atrophy  of  certain 
groups  of  muscles,  and  after  a  time  the  pseudo-hypertrophy  disappears 
and  atrophy  takes  its  place.  In  the  lower  limbs  the  muscles  most 
atrophied  are  the  flexors  of  the  hips,  then  the  extensors  of  the  knee  and 
those  of  the  hip.  The  calf  muscles  fail  before  the  anterior  tibial.  The 
atrophy  and  consequent  weakness  of  the  lower-limb  muscles  cause  great 
difficulty  in  going  upstairs,  the  gait  becomes  more  waddling,  and  the 
patient  loses  the  power  of  getting  up  when  lying  on  the  floor  or  he  climbs 


Fig.  142. — Pseudo-muscular  hypertrophy,  patient  "chmbing  up  the  legs." 


up  his  legs  (Fig.  142).  These  peculiarities  are  due  chiefly  to  the  weakness 
in  the  extensors  of  the  knees,  the  extensors  of  the  hip,  the  flexors  of  the 
hip  and  the  erector  spinse.  By  reason  of  the  same  defects,  the  child  when 
standing  has  an  antero-posterior  curvature  of  the  spine  with  the  con- 
cavity backward  (lordosis)  (Fig.  141).  This  is  clue  to  the  weakness  of 
the  extensors  of  the  hips,  which,  acting  from  the  hips,  are  unable  to  tilt 
the  pelvis  back.  On  sitting,  this  lordosis  disappears  and  is  replaced  often 
by  a  curve  in  the  opposite  direction  due  to  weakness  of  the  erectors  of 
the  spine.  There  may  be  some  lateral  curvature  also.  In  consequence 
of  the  weakness  and  contractures  of  the  leg  muscles,  there  early  develops 
a  talipes  equinus,  and  later  the  legs  may  become  flexed  on  the  hips  and 
the  forearms  on  the  arms. 

The  muscles  show  no  fibrillary  twitching  and  rarely  any  degenerative 


312 


DISEASES    OF    THE    NERVOUS    SYSTEM 


reactions,  but  there  is  sometimes  a  peculiar  tetanic  contraction  with  both 
the  faradic  and  the  galvanic  current.  A  myotonia  occasionally  develops 
on  the  basis  of  a  dystroyhy. 

The  knee-jerks  and  elbow-jerks  gradually  weaken  and  in  time  are 
lost. 

There  is  no  pain  or  other  disturbance  of  sensibility. 
The  affected  parts  feel  cold  and  look  reddened,  as  if  from  deficient 
vasomotor  innervation.     The  organic  spinal  centres  are  not  involved. 
Intelligence  is  usually  good. 

Course.^ — The  disease  runs  a  chronic  but  variable  course.  Its  prog- 
ress is  at  first  slow,  and  after  walking  becomes 
impossible  it  may  cease  to  progress.  It  lasts 
from  ten  to  twenty-five  years.  In  a  few 
cases  patients  have  reached  the  age  of  fifty 
or  sixty  years,  even  when  the  disease  began 
in  youth.  The  earlier  the  disease  begins  the 
more  rapidly  it  extends;  the  more  pronounced 
the  tendency  to  lipomatosis,  the  more  rapid 
is  the  course. 

Pathological  Anatomy .^ — The  disease,  like 
other  forms  of  dystrophy,  is  a  degenerative 
atrophy,  the  process  affecting  first  the  muscle 
fibres  and  nerve  terminals,  the  connec- 
tive tissue  being  secondarily  involved.  In 
a  simple  atrophy  of  muscles,  such  as  follows 
disuse,  the  muscle  fibres  grow  smaller  and 
gradually  break  up  and  disappear.  In  de- 
generative atrophy,  the  process  is  accom- 
panied by  evidences  of  irritation,  such  as 
swelling  of  the  muscle  fibre,  proliferation  of 
muscle  nuclei,  splitting  of  the  fibre  longi- 
tudinally, and  connective  tissue  proliferation.  All  these  phenomena 
are  seen  in  the  pathological  process  which  takes  place  in  the  dystro- 
phic muscles.  All  the  varied  changes  may  be  noted  in  the  same  mus- 
cle. In  the  early  stages  there  is  a  true  hypertrophy  of  some  of  the 
fibres,  a  condition  thought  to  be  characteristic  of  the  muscular  dys- 
trophies in  distinction  from  the  spinal  atrophies.  Besides  swelhng  and 
hypertrophy  of  fibres,  one  sees  atrophy  of  the  fibres;  the  bundles  are 
rounded;  there  are  increase  of  muscle  nuclei,  splitting  of  fibres,  vacuoliza- 
tion, and  a  tendency  to  break  up  into  fibrillse  (Erb).  The  connective 
tissue  at  first  shows  evidence  of  irritation  and  proliferation.  Finally, 
as  the  muscular  atrophy  progresses,  connective  tissue  increases  and  takes 
its  place,  until  a  dense,  hard  myosclerosis  results  (Figs.  145, 146).     In  some 


Fig.  143. — Leyden-Moebius 
type  of  dystrophy.  {Schcenborn 
and  Krieger.) 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES 


313 


parts  there  is  deposit  of  fat  in  the  connective-tissue  cells,  and  this  may 
increase  until  an  extensive  lipomatosis  exists.  In  the  later  stage  of  the 
disease  the  fat  deposits  are  absorbed  and  there  are  only  atrophied  muscle 


Fig.  144.- — Cross-section  of  crural  muscle  in  dystrophy,  showing  hj^pertrophied  and 
atrophied  fibres,  increase  of  nuclei.      (Cestan  and  Lejo?ine.) 

and  connective  tissue.     The  nerves  and  spinal  cord  are  usually  normal; 
when  changes  are  found  they  are  secondary  to  the  muscular  disease. 

The  process  is  then,  first,  hypertrophy  of  muscle  fibre  and  increase  of 
muscle  nuclei,  swelling  and  rounding  of  fibres,  and  splitting  of  the  same; 


-f£^<^jLi  x^_;_ 


^r-^-.^  -^ '- 


"in^- 


'^ 


.t^i*^— SV         *"' 


Wr^;'—  ■~;^'\.~'~:_ 


Fig.  14,5. — Longitudinal  section  of  supinator  longus  in  dystrophy  showing  atrophic 
fibres  and  fat.     {Cestan  and  Lejonne.) 

then  increase  of  connective  tissue,  with  corresponding  atrophy  of  muscle 
and  deposit  of  fat. 

The  process  is  a  primary  degeneration  due  to  an  inherent  nutri- 


314 


DISEASES    OF    THE    NERVOUS    SYSTEM 


il. 


tional  weakness  of  the  muscle.     In  a  measure  it  is  true  that  those  muscles 
embryologically  latest  developed  are  earliest  attacked. 

The  juvenile  dystrophy  of  Erh,  or  scapulo-humeral  form  of  dystrophy 
(root  dystrophy) ,  begins  in  childhood  or  early  youth,  a  little  later  than 

pseudo-hypertrophy.  The  shoulder- 
girdle  is  first  affected,  later  the  arm. 
The  forearm  and  legs  are  attacked 
very  late.  Part  of  the  pectorals,  part 
of  the  trapezii,  latissimus  dorsi,  rhom- 
boid, upper-arm  muscles  and  supina- 
tors are  affected,  while  the  supra-  and 
infraspinati  and  forearm  and  hand 
usually  escape.  There  may  be  true 
and  false  muscular  hypertrophy. 
There  are  no  fibrillary  contractions  or 
degenerative  reactions  (Fig.  146). 

As  the  disease  progresses  it  grad- 
ually affects  the  hip-girdle  and  trunk, 
and  finally  the  patients  have  an  al- 
most general  atrophy.  This  is  then 
the  root  and  trunk  dystrophy,  which  I 
find  the  common  one  in  this  country. 
The  facio-scapulo-humeral  form,  or 
infantile  progressive  muscular  atro- 
phy begins  in  early  childhood  (third, 
or  fourth  year)  usually,  but  may  de- 
velop late.  The  atrophy  attacks  first 
the  face,  giving  a  characteristic  ap- 
pearance known  as  the  "myopathic 
face."  There  is  a  weakness  of  the 
oral  muscle,  which  causes  the  lips  to 
protrude  and  produces  a  symptom 
called  the  ''tapir  mouth."  The 
atrophy  respects  the  eye  muscles  as 
well  as  those  of  mastication  and  deglu- 
tition. It  extends  to  the  shoulders 
and  arms  next,  then  it  pursues  the 
ordinary  course  of  the  dystrophies. 
Prognosis. — The  patient  never  re- 
covers, but  the  disease  sometimes  comes  to  a  standstill  and  there 
may  even  be  some  improvement,  especially  in  cases  beginning  late. 

Treatment. — The    prophylaxis    is    important.     It    consists    in    pre- 
venting the  marriage  of  women  belonging  to  dystrophic  families;  if  a 


Tig.  14G. — Juvenile  lype  oi"  pro- 
gressive muscular  dystrophy ;  sixth  year 
of  disease. 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES  315 

dystrophy  has  developed  in  one  child,  it  would  be  unwise  to  take  the 
risk  of  bringing  others  into  the  world.  Or  if  children  are  already  born, 
they  should  receive  the  most  careful  nourishment,  outdoor  life  should 
be  secured,  and  the  dangers  from  trauma  and  the  infective  diseases  be 
prevented.  Infants  should  not  be  suckled  by  the  mother  if  she  belongs 
to  the  dystrophic  family. 

The  moderate  use  of  massage  and  gymnastics  is  very  important 
and  useful.  All  kinds  of  tonic  measures  are  indicated,  such  as  cold 
baths,  good  nourishment,  arsenic,  strychnine,  and  phosphorus  and  fats. 
Tenotomy  and  other  orthopaedic  measures  may  be  useful  in  the  later 
stages.     Feeding  with  thymus  or  other  glands  does  no  good. 

Amyotonia  congenita  or  myatonia  congenita  is  a  condition  described 
by  Oppenheim  and  later  by  Spiller  and  others.  It  occurs  in  childhood 
and  is  associated  with  great  weakness,  flaccidity  and  atony  of  the  muscles 
of  the  lower  and  sometimes  of  the  upper  extremity.  The  limbs  may  be 
moved  like  flails;  the  muscles  are  not  apparently  wasted,  but  react  poorly 
to  electrical  stimulation.  The  reflexes  are  weakened  or  lost.  Active 
movements  are  feeble  but  not  entirely  lost. 

The  disease  is  congenital  and  in  some  cases  may  be  the  result  of  ac- 
cident of  intra-uterine  life.  There  is  no  history  of  heredity.  In  mild 
cases  the  disease  seems  to  be  a  purely  muscular  one;  in  severer  cases  the 
central  nervous  system  is  involved.  So  it  is  still  a  question  as  to  whether 
it  should  be  classed  among  the  muscular  dystrophies. 

UNILATERAL  HYPERTROPHY  OF  THE  FACE 

Dr.  D.  W.  Montgomery  has  collected  nine  cases  of  this  affection, 
seven  being  congenital  and  one  commencing  in  the  second  year  of  life. 
One  followed  a  neuralgia  of  the  fifth  nerve.  Dr.  Montgomery  reported 
a  case  in  which  the  development  began  at  the  age  of  ten  years.  In  this 
case,  the  hypertrophy  involved  the  bone,  and  it  seems  to  have  been  a  type 
of  leontiasis  ossea. 

HEMIHYPERTROPHY 

There  have  been  reported  in  literature  by  Mobius,  Demme,  and  C.  B. 
Tilanus  a  few  cases  of  hypertrophy  of  one  side  of  the  body.  In  one 
case,  the  child  was  born  with  a  half-sided  muscular  hypertrophy.  In 
the  other  cases,  the  disease  seems  to  have  been  also  of  congenital  origin. 
The  trouble  seems  to  be  a  kind  of  teratological  defect,  and  not  due 
to  any  progressive  disorder  of  the  muscular  system. 

SUMMARY  OF  THE  HEREDITARY  OR  FAMILY  NERVOUS  DISEASES 

The  student  may  well  be  confused  by  the  large  number  of  so-called 
family  nervous  diseases  which  modern  neurology  has  discovered  and 


316  DISEASES    OF    THE    NERVOUS    SYSTEM 

differentiated.  The  practical  importance  of  them  all  is,  perhaps,  slight, 
for  they  are  extremely  rare,  j^et  it  is  necessary  that  they  be  recognized 
and  properly  distinguished,  for  the  prognosis  and  degree  of  suffering 
differ  very  much  in  different  cases.  They  are  all  chracterized  by  the 
fact  that  they  are  found  in  different  generations  and  in  different  collateral 
branches  of  a  given  family,  and  that  they  are  not  necessarily  or  often 
passed  on  directly  from  one  parent  to  another.  The  list  which  I  append 
contains  the  important  types. 

Hereditary  Chorea. — This  is  really  a  kind  of  hereditary  paresis  or 
brain  softening.  It  does  not  develop  until  adult  life,  as  a  rule,  and 
patients  with  it  may  live  until  middle  age. 

Hereditary  amaurotic  idiocy  is  a  family  disease,  early  described  by 
Dr.  Sachs,  characterized  by  a  general  degeneration  of  all  the  nerve- 
cells  of  the  central  nervous  system  associated  with  blindness  and  a 
peculiar  degeneration  of  the  optic  nerves. 

Hereditary  Cerebral  Diplegia. — ^This  is  a  family  disease  in  which 
children  between  the  ages  of  one  and  five  develop  spastic  paralysis  and 
sometimes  imbecility. 

Hereditary  Hemiplegia. — ^This  is  a  family  disease  which  has  been 
referred  to  by  Hoffmann  and  of  which  I  have  seen  two  cases  in  my 
clinic.  The  children  are  born  hemiplegic  and  there  is  atrophy  of  the 
hemiplegic  side,  but  in  my  cases  there  was  no  mental  defect  or  epilepsy. 

Hereditary  cerebellar  ataxia  is  a  disease  allied  to  Friedreich's  ataxia, 
but  developing  somewhat  later;  i.e.,  about  the  time  of  puberty. 

Hereditary  spinal  ataxia,  or  Freidreich's  disease,  is  fully  described 
elsewhere. 

Hereditary  Spastic  Spinal  Paralysis. — Spastic  paralysis  in  very  rare 
cases  is  found  to  run  in  famihes,  affecting  different  members  of  many 
succeeding  generations.  In  the  cases  described,  it  begins  at  about 
the  age  of  five,  affects  only  or  mainly  the  legs,  runs  a  very  slow  course,  is 
not  accompanied  by  pain,  ataxia  or  visceral  symptoms;  and  runs  a 
course  lasting  twenty  or  thirty  years. 

Hereditary  progressive  Spinal  Muscular  Atrophy. — There  is  (a)  an  in- 
fantile form  (Werding-Hoffmann  type)  and  {h)  a  form  beginning  in 
in  middle  life  or  later,  described  by  the  writer. 

Hereditary  Muscular  Atrophy  of  Peroneal  Type  (Charcot-Marie 
Tooth). — This  has  been  described  under  the  spinal  atrophies. 

Hereditary  progressive  dystrophies  include  a  large  number  of  types 
as  above  described. 

ARTHRITIC  MUSCULAR  ATROPHY 

In  inflammation  of  joints  the  muscles  moving  them  are  affected  by  a 
simple  atrophy  which  is  called  arthritic. 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES  317 

Etiology. — Rheumatic  arthritis  is  the  commonest  cause. 

Symptoms. — The  shoulder-girdle  muscles  are  oftenest  affected,  next 
the  muscles  of  the  thighs  and  legs.  Whatever  the  joint,  it  is  the  extensor 
muscles  which  are  first  and  most  attacked,  while  the  muscles  above  the 
joint  are  more  susceptible  to  the  atrophy  than  those  below.  The  atrophy 
is  rather  rapid  in  the  first  few  weeks  and  then  becomes  slower.  The 
muscles  affected  waste  throughout  their  whole  length.  Thej^  show  no 
fibrillary  contractions  and  no  degenerative  electrical  reaction.  There  is 
often  an  increased  irritability,  so  that  an  exaggerated  tendon  reflex  or 
even  clonus  may  be  produced.  There  is  no  pain  or  tenderness  or  anaes- 
thesia in  the  muscles, 

Pathology. — -The  anatomical  change  is  a  simple  atrophy  and  shrink- 
ing of  the  muscle  fibres,  with  some  increase  in  muscle  nuclei,  little  vacuola- 
tion,  no  swelling  or  splitting  of  fibres  (Darkschewitch) .  There  is  some 
increase  in  interstitial  tissue,  but  this  is  slight.  The  nerves  and  spinal 
cord  are  normal. 

The  atrophy  is  probably  due  in  part  to  disuse  and  in  part  it  is  a  reflex 
trophic  disturbance. 

The  prognosis  is  good.  If  the  arthritis  gets  well  the  muscles  are  also 
restored. 

The  treatment  consists  of  electricity  and  gentle  massage,  exercise  and 
internal  remedies  directed  to  the  arthritis. 

OCCUPATION  MUSCULAR  ATROPHIES 

As  a  result  of  constant  over-use,  muscles  sometimes  atrophy.  This 
applies  especially  to  the  smaller  muscles  of  the  hand.  Thus  there  occurs 
an  atrophy  of  the  thenar  eminence  in  lapidaries  and  in  persons  who 
constantly  use  this  group  of  small  muscles. 

Typical  atrophies  of  this  kind  may  be  seen  in  persons  who  run  ele- 
vators and  who  have  constantly  to  grasp  the  rope  in  one  hand;  in  golfers 
who  use  a  special  grip;  in  artisans  who  have  to  use  excessive  pressure 
on  motor  nerves.  The  biceps  sometimes  wastes  in  smiths  and  the  calf 
muscles  in  ballet  dancers.  In  most  cases  this  occupation  atrophy  of 
muscles  reaches  a  certain  stage  and  stops.  If  the  patient  is  given  rest, 
recovery  takes  place.  This  is  especially  true  if  the  patient  is  young 
and  in  vigorous  health.  In  other  instances,  the  simple  occupation  atrophy 
will  actually  pass  over  into  progressive  muscular  atrophy.  The  trouble 
is  usually  due  to  a  local  neuritis  caused  by  trauma. 


CHAPTER  XV 


TUMORS  AND  CAVITIES  OF  THE  SPINAL  CORD 


Frequency  and  Cause. — ^Tumors  of  the  spinal  cord  occur  about  one- 
half  as  often  as  tumors  of  the  brain.  Among  1,000  nervous  cases  there 
will  be  an  average  of  one  or  two  spinal  tumors.  Men  are  affected  oftener 
than  women.  The  susceptible  age  is  that  of  middle  and  active  life. 
Children  do  not  often  have  spinal  tumors  and  old  people  have  only  the 
metastatic  and  secondary  type.  Injuries  to  the  back  are  sometimes  the 
exciting  cause.  Naturally,  the  presence  in  the  system  of  cancer,  sarcoma, 
tuberculosis  and  Hodgkin's  disease  is  a  predisposing  cause  of  deposits  in 
the  cord. 

Location. — Tumors  of  the  spinal  cord  are: 

/  Cancer. 


Extra-dural. 


Intra-dural. 


1.  Vertebro-spinal. 

2.  Spinal. 

3.  Extra-medullary. 

4.  lntra-medullarJ^ 


\  Sarcoma.. 

/  Sarcoma,  fibroma. 

Neuroma,  lipomata. 

Lipoma,  neuroma. 

Fibroma,  sarcoma. 

Tubercle,  cysts,  etc. 

Endothelioma. 
Sarcoma. 
Glioma. 
[  Cancer,  etc. 

All  parts  of  the  spinal  cord  are  attacked,  the  cervical  region,  however, 
is  most  frequently  involved  and  next  in  nearly  the  same  frequency  are 
the  conus  and  cauda  equina.  Then  come  the  lower  part  of  the  dorsal 
cord,  the  upper  part  of  the  dorsal  cord  and  last  of  all  the  lumbar  and  upper 
sacral  cord.  The  figures  representing  the  proportional  distribution  would 
be  somewhat  as  follows: 

Cerical 7     Upper   dorsal S}4 

Conus    and  cauda 6     Lumbar 2 

Lower  dorsal 5 

The  relative  frequency  of  the  different  forms  of  tumors  is  shown  in 
the  following  table  of  personal  cases  of  vertebro-spinal  and  spinal 
tumors : 


Sarcoma 24 

Carcinoma 12 

Glioma 9 

Endothelioma 4 


Tuberculoma 2 

Cyst 2 

Neuro-fibroma 2 

Adenoma 1 


318 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES  319 

If  one  leaves  out  from  this  table  the  vertebro-spinal  tumors  the  rela- 
tive frequency  would  be  about  the  same,  except  for  the  carcinomata. 

The  most  frequent  form  of  tumor,  as  is  seen  above,  is  the  sarcoma; 
next  to  this  the  carcinoma,  glioma  and  endothelioma.  The  sarcoma 
undergoes  various  changes  and  is  sometimes  osteosarcoma,  sometimes 
fibrosarcoma,  gliosarcoma  or  endosarcoma.  The  endothelioma  is  a 
common  tumor  or  not,  apparently,  according  to  the  laboratorj^  in  which 
it  is  examined.  A  number  of  sarcomata  are  considered  by  some  authori- 
ties to  be  endotheliomata. 

Tuberculoma  is  relatively  rare  and  syphiloma  is  a  tumor  that  I  have 
never  seen  and  has  been  rarely  reported  in  this  country. 

If  one  groups  glioma  (which  is  the  cellular  type  of  glioma  prolifera- 
tion) with  syringomyelia  (which  is  a  fibril  stage  of  proliferation)  we  would 
probably  find  that  the  most  frequent  form  of  new  growth  which  attacks 
the  spinal  cord  is  gliomatosis  in  some  form. 

Cysts  and  fibromata,  parasites  and  adenoma  are  rare  and  almost 
curiosities  in  the  pathological  laboratories  of  neurologists. 

VERTEBRO-SPINAL  TUMORS 

Nature  and  Frequency. — The  tumors  of  the  vertebral  column,  which 
later  involve  the  cord,  are  carcinoma,  and  less  often  sarcoma  or  osteo- 
sarcoma. Carcinoma  is  almost  invariably  of  metastatic  origin,  the 
primary  source  being  oftenest  the  breast,  less  often  the  stomach,  uterus 
and  prostate.  Sarcomatous  tumors  may  be  primary.  Other  forms  of 
vertebro-spinal  tumor  are  very  rare.  They  are  myoma,  osteoma, 
enchondroma  and  cysts. 

The  tumors  of  the  spinal  cord  which  originate  in  the  spinal  canal 
outside  the  dura  mater,  but  do  not  start  from  the  vertebrae,  are  lipoma, 
which  is  congenital,  fibroma,  hydatid  cysts,  tuberculoma,  neuroma  and 
sarcoma. 

In  my  list  of  forty-seven  tumors  involving  the  cord,  about  10  per  cent, 
were  carcinoma  or  sarcoma  and  of  vertebro-spinal  character.  About  12 
per  cent,  were  extra-dural  but  not  of  vertebral  origin.  The  remainder 
were  intra-dural  tumors  and  were  either  of  meningeal  origin  or  were 
intra-medullary  and  of  gliomatous  character. 

Symptoms  and  Course. — Vertebro-spinal  tumors  occur  oftenest  in 
later  life,  although  sarcoma  may  occur  early.  Several  of  the  vertebrae 
are  usually  involved.  The  bony  tissue  becomes  softened  and  destroyed 
and  a  kyphosis  occurs.  This  is  not  sharp  and  angular  as  in  Pott's  disease, 
but  is  more  rounded.  As  the  disease  progresses  it  involves  the  nerve- 
roots  and  cord,  causing  local  pain,  rigidity  of  the  spinal  muscles,  spasmodic 
twitchings,  later  anaesthesia,  paraplegia  and  loss  of  control  of  the  sphincters ; 


320  DISEASES    OF    THE    NERVOUS    SYSTEM 

vasomotor  and  trophic  disturbances  also  develop.  In  fine,  the  symptoms 
are  like  those  of  tumors  of  the  spinal  cord,  to  be  described  later,  beginning 
with  local  pain  and  irritation  and  ending  in  a  transverse  or  diffuse 
destruction  of  the  nervous  centres.  The  disease  is  very  painful  and 
often  progresses  rapidly,  but  remissions  may  occur. 

Diagnosis. — The  history  of  a  primary  malignant  disease,  the  exces- 
sive pain,  tenderness  of  the  vertebra  to  jarring,  then  the  rounded  kyphosis, 
the  progressive  development  of  irritative  and  later  of  paralytic  changes 
due  to  involvement  of  the  cord  make  the  diagnosis  easy.  The  X-ray 
is  often  of  decisive  value.  Examination  of  the  cerebrospinal  fluid  is 
useful  especially  in  excluding  syphilis  and  inflammatory  changes.  The 
condition  must  be  differentiated  especially  from  tuberculosis  of  the  spine 
and  from  spinal  softening  due  to  toxic  conditions. 

In  the  cases  of  sarcoma,  operation  is  sometimes  helpful.  I  have  seen 
apparent  cure  by  the  use  of  Coley's  toxins.  The  value  of  radium  and 
of  cross-firing  with  X-rays  has  yet  to  be  established. 

SPINAL  CORD  TUMORS  PROPER 

Extra-dural  tumors  of  the  spinal  cord  are  about  as  frequent  as  intra- 
dural tumors.  If,  however,  we  leave  out  the  vertebral  tumors  we  find  that 
neoplasms  starting  within  the  dura  are  at  least  five  times  as  frequent  as 
those  starting  from  or  involving  its  outer  surface. 

Of  the  tumors  that  start  within  the  dura  some  originate  from  the 
meninges  and  some  within  the  cord  itself.  Those  originating  from  the 
meninges  are  rather  more  numerous.  This  statement  would  not  be  true, 
however,  if  we  included  under  this  head  cases  of  syringomyelia.  In- 
cluding this  disease,  in  my  experience  gliomatous  tumor  is  the  most 
frequent  of  all  forms  of  those  originating  within  the  dura  mater.  This 
would  correspond  with  Cushing's  experience  with  brain  tumors.  He 
found  that  65  per  cent,  of  these  were  of  gliomatous  character. 

Symptoms. — No  disease  of  the  spinal  cord  offers  such  a  varying  and 
often  baffling  group  of  symptoms  as  does  that  of  spinal  tumor;  at 
least  this  is  true  of  perhaps  10  per  cent,  of  the  cases.  In  the  remainder 
of  more  or  less  typical  cases  the  general  symptoms  are  about  as  follows: 

First,  there  is  a  group  of  symptoms  extending  from  a  certain  fixed 
point  in  the  spinal  cord  and  rather  steadily  progressing  for  a  period  of 
months.  Second,  these  symptoms  are  usually  at  first  unilateral  and 
then  extend  to  the  other  side.  Third,  the  symptoms  are  those  of  pressure 
and  irritation  with  intense  pain  and  signs  of  motor  irritation,  such  as 
twitching  and  rigidity,  followed  later  by  symptoms  of  cord  injury  due  to 
pressure  and  disintegration  of  the  cord,  causing  paralysis,  atrophy  and 
loss  of  sphincter  control.     Fourth,  there  is  evidence  of  total  disintegra- 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES  321 

tion  of  the  cord  at  a  certain  level,  and  associated  with  this  are  some 
evidences  of  bonj'-  disturbance,  such  as  tenderness  and  rigidity  and  change 
in  the  percussion  note.  These  general  symptoms  vary  with  the  location, 
character,  size  and  rate  of  growth  of  the  tumor.  Pain  appears  early  and 
is  a  very  frequent  but  not  invariable  symptom.  It  is  severe  and  shooting 
and  is  of  the  root-pain  character,  being  not  distributed  along  different 
peripheral  nerves  but  according  to  segments.  There  is  usually  a  girdle 
sensation.  In  tumors  of  the  cervical  region  this  is  often  felt  several 
segments  below  the  level  of  the  tumor.  Numbness,  hypersesthesia  and 
later  anaesthesia  below  the  level  of  the  lesion  occur.  In  intra-meduUary 
tumors  the  symptoms  may  ascend.  There  is  tenderness  over  the  spine 
and  rigidity  at  times.  As  the  tumor  increases,  spastic  conditions  of  the 
extremities  develop,  involving  one  or  both  legs  or  an  arm  and  leg,  later 
paraplegia,  atrophy  and  loss  of  control  of  the  bladder  and  rectum  with 
bed-sores;  then  death  ensues  from  exhaustion. 

When  the  disease  is  cervical,  first  one,  then  the  other  upper  ex- 
tremity is  involved,  with  evidence  soon  of  implication  of  the  pyramidal 
tracts.  Then  the  legs  become  weak  and  stiff.  The  ciliary  centre  may  be 
irritated  or  paralyzed  if  the  tumor  is  in  the  lower  cervical  or  first  dorsal 
region.  If  lower  down,  there  develops  a  hemiparaplegia,  later  a  complete 
paraplegia,  usually  with  exaggerated  reflexes.  If  the  tumor  is  in  the 
lumbar  region  the  reflexes  are  sooner  lost  and  the  sphincters  early  involved. 
In  that  site  the  tumor  gradually  grows  and  symptoms  progress  until 
the  patient  becomes  paralyzed  with  anaesthesia,  contractures,  loss  of 
sphincter  control,  bed-sores  and  finally  death  from  intercurrent  disease  or 
exhaustion. 

A  rather  frequent  type  of  symptoms  caused  by  spinal  tumors,  and 
occasionally  by  injuries  and  syphilis,  is  that  known  as  a  Brown-Sequard 
jjaralysis  or  hemiparaplegia.  In  a  typical  case  of  this  kind  there  are 
paralysis  of  motion  and  muscle  sense  with  exaggeration  of  deep  reflexes 
on  the  side  of  the  lesion,  paralysis  of  cutaneous  sensation,  especially  of 
pain  and  of  temperature  on  the  opposite  side  up  to  just  below  an  anaes- 
thetic band  on  the  side  of  the  lesion.  On  the  side  of  the  lesion  the  tem- 
perature may  be  slightly  raised  and  there  is  often  hyperaesthesia.  There 
may  be  a  band  of  anaesthesia  at  the  level  of  the  lesion  and  on  the  same  side 
(Fig.  147).     The  symptoms  may  be  grouped  as  follows: 

On  the  side  of  the  lesion: 

1.  Paralysis  more  or  less  complete. 

2.  Diminution  of  deep  sensibility. 

3.  Tactile  hyperaesthesia. 

4.  Vasomotor  paralysis. 

5.  Sometimes  a  band  of  cutaneous  anaesthesia  just  at  the  site  of  the 
lesion. 

21 


322 


DISEASES    OF   THE    NERVOUS    SYSTEM 


On  the  side  opposite  the  lesion: 

1.  Diminution  of  cutaneous  sensation,  especially  pain  and  thermic. 
If  the  lesion,  however,  is  low  in  the  lumbar  and  sacral  cord  there  is 
anaesthesia  of  both  sides. 

If  the  lesion  is  in  the  cervical  region  there  will  be  a  spinal  hemiplegia, 

and  perhaps  pupillary  changes. 

The  diagnosis  of  vertebro-spinal  tu- 
mors from  the  extra-  and  intradural  is 
not  always  possible.  Root  pains  which 
begin  unilaterally  and  later  become  bi- 
lateral indicate  tumor  of  the  spinal 
meninges.  However,  when  extra-medul- 
lary growths  lie  in  front  of  the  cord 
there  may  be  no  pain,  and  if  tumors 
involve  the  anterior  roots  there  will  be 
muscular  atrophy  of  the  root  distribution. 
In  extra-medullary  tumors  there  is 
apt  to  be  more  evidence  of  irritation  such 
as  increased  amount  of  pain  and  reflex 
spasm  of  the  lower  limbs. 

The  Brown-Sequard  syndrome  may 
be  due  to  a  tumor  either  outside  or  in- 
side the  dura,  but  it  is  usually,  at  least, 
extra-medullary. 

Experience  has  shown  that  there  is  a 
tendency  to  localize  the  spinal  tumors 
below  the  level  where  they  actually  lie 
and  it  is  absolutely  important  to  make 
very  careful  tests  as  to  the  existence  of 
hypersesthesia,  and  anaesthesia  in  order 
to  be  sure  of  the  tumor  level.  The  ex- 
istence of  definite  root  pains  correctly 
localized  or  of  definite  anaesthesia  of  the 
root  type  is  characteristic  of  a  tumor 
and  distinguishes  it  from  local  meningitis. 
The  duration  of  life  in  cases  of  spinal  tumor  ranges  from  three  to 
five  years. 

Pathological  Anatomy. — This  subject  has  been  dealt  with  in  the 
general  introduction. 

Spinal  tumors  are  small  in  size,  ranging  from  one-fifth  to  one  and 
one-fifth  inches  (one-half  to  three  centimeters)  in  diameter.  The  glioma 
may  diffuse  for  a  long  distance  through  the  centre  of  the  cord,  forming 
cavities  (syringomyelia).     The  sarcomatamay  likewise  be  irregularly 


Fig.  147. — Showing  the  condi- 
tion in  a  Brown-Sequard  paralysis 
due  to  a  tumor  growing  in  the  left 
side  of  the  spinal  cord.  On  the  left 
side,  hypersesthesia,  ataxia,  paraly- 
sis, exaggerated  reflexes.  At  the 
upper  limit  is  a  band  of  anaesthe- 
sia.    On  right  side,  anaesthesia. 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES 


323 


spread  along  the  surface  of  the  cord.     Spinal  tumors  are  usually  single, 
but  fibromata,  the  parasites,  cancer  and  sarcomata  may  be  multiple. 

Diagnosis. — The  disease  has  to  be  distinguished  from  vertebral  caries, 
localized  serous  cysts,  transverse  myelitis,  syphilitic  meningitis  and 
pachymeningitis.  The  points  to  be  noted  as  regards  caries  are  the  ab- 
sence of  an  angular  deformity  or  kyphosis;  the  small  degree  of  pain, 
tenderness  and  rigidity,  absence  of  anaes- 
thesia, the  age  and  the  absence  of  tuber- 
cular diathesis.  The  slowly  progressive 
course,  beginning  with  pain,  the  one-sided 
motor  and  sensory  paralysis  and  the 
localization  of  the  symptoms  exclude 
myelitis.  Lumbar  puncture  may  help  in 
diagnosis  by  exclusion.  The  fluid  shows 
no  cells,  but  is  often  of  a  greenish-yellow 
tinge  and  has  excess  of  globulin  but  no 
excess  of  cells. 

The  character  of  the  tumor  cannot 
often  be  determined  certainly.  The 
probabilities  are  in  favor  of  sarcoma  or 
glioma,  especially  in  middle  life.  Syphil- 
oma may  be  determined  from  the  history 
and  results  of  lumbar  puncture.  Tubercu- 
loma is  very  rare,  and  is  more  likely  to 
occur  in  the  young. 

Prognosis.— This  is  not  good.  Medi- 
cine is  of  little  use  except  in  syphiloma,  and 
even  here  it  may  be  ineffective.  Tubercle 
may  perhaps  cease  to  grow.  Surgical  in- 
terference now  saves  the  life  of  some  pa- 
tients and  is  a  more  hopeful  form  of  in- 
terference on  the  whole  than  in  cerebral 
tumors.  This  is  more  true  now  than  ten 
years  ago.  Out  of  eight  rather  recently 
operated  cases,  there  were  excellent  re- 
sults in  five.  These  were,  to  be  sure,  selected  cases  of  intradural  or  non- 
vertebral  tumors. 

Treatment.- — In  syphilitic  tumors  appropriate  remedies  may  do  good 
and  should  be  vigorously  used.  In  tubercle,  bodily  rest,  tonic  treatment, 
iodine  and  cod-liver  oil  may  be  of  service.  In  gliomata  and  sarcomata, 
arsenic  may  be  tried.  In  other  forms,  symptomatic  treatment  is  all 
that  can  be  recommended  medically.  In  all  cases  of  spinal  tumor  surgical 
interference  should  be  considered ;  extra-dural  and  extra-medullary  tumors 


Fig. 


148. — Sarcoma   of  cord  and 
cervical  region. 


324 


DISEASES    OF   THE    NERVOUS   SYSTEM 


can  often  be  removed  with  success  and  also  with  benefit  to  the  patient. 
In  medullary  tumors  operations  have  been  successfully  done  by  the 
process  of  incising  the  cord  and  allowing  the  tumor  to  extrude  ("decom- 
pression method  of  Elsberg). 

The  use  of  radium  and  cross-firing  with  X-ray  may  prove  to  be 
helpful. 

CAVITIES  IN  THE  SPINAL  CORD 

The  cavities  of  the  spinal  cord  are  known  as: 

1.  Hydroinyelia. 

2.  Myelitic  cavities. 

3.  Syringomyelia. 

There  may  be  various  combinations  of  those  processes,  the  most 
common  being  a  combination  of  hydromyelia  and  syringomyelia. 

HYDROMYELIA 

This  is  a  dilatation  of  the  central  canal  of  the  cord,  the  cavity  being 
filled  with   fluid   (Fig.   149).     The    condition   may  be  associated  with 


Fig.   149. — Hydromyelia. 

hydrocephalus  or  with  spina  bifida,  or  it  may  be  independent  of  these 
conditions.  The  dilatation  may  be  cystic  and  irregular,  or,  as  is  more 
usual,  may  extend  throughout  the  cord.  The  dilatation  extends  more 
posteriorly,  because  the  posterior  columns  are  formed  latest.  The  abnor- 
mality may  be  slight  and  give  rise  to  no  symptoms,  or  a  pathological 
process  like  a  gliomatosis  may  develop  upon  it. 

MYELITIC  AND  HEMORRHAGIC  CAVITIES 

Such  cavities  may  be  formed  in  the  cord  by  a  central  excavating 
myelitis  or  by  small  hemorrhages.     These  cavities  are  usually  small. 


MUSCULAR   ATROPHIES    AND    DYSTROPHIES 


325 


irregularly   distributed,   and   are  lined   with   connective  tissue.     They 
may  be  formed  in  rare  cases  in  connection  with  hydromyelia  or  neoplasms. 


GLIOSIS  AND  SYRINGOMYELIA 

Syringomyelia  is  a  disease  of  the  spinal  cord  characterized  by  a 
development  of  gliomatous  tissue  in  the  central  parts  with  formation 
of  cavities.  Such  cavities  are  not  always  formed,  however,  and  then  the 
condition  is  known  as  spinal  gliosis.  Clinically  the  condition  is  charac- 
terized by  the  slow,  progressive  development  of  a  muscular  atrophy  with 
peculiar  disturbances  of  sensation  and  of  vasomotor  function. 


Fig.  150. — Distribution  of  cutaneous  anaesthesia  in  syringomyelia.  1  shows  area 
of  analgesia,  2  shows  that  of  thermo-ansesthesia.  The  darker  shades  show  where 
there  is  anaesthesia  to  pain  and  temperature,  the  tactile  sense  being  unimpaired. 

Etiology. — The  disease  is  rare.  It  is  more  frequent  than  amyotro- 
phic lateral  sclerosis  and  less  frequent  than  multiple  sclerosis.  It  occurs 
oftener  in  men  than  in  women,  and  develops  in  early  and  middle  life, 
between  the  ages  of  fifteen  and  forty-five.  It  occurs  especially  in  persons 
who  follow  hard  manual  occupations,  such  as  butchers,  tailors,  etc. 
Traumatism  is  the  most  important  exciting  factor  in  my  experience. 
There  is  sometimes  an  underlying  teratological  defect  in  the  cord.  In- 
fectious diseases  seem  occasionally  to  start  up  the  trouble.  Heredity, 
syphilis  and  alcohol  are  not  causal  factors. 

Symptoms. — The  disease  begins  insidiously  with  some  aching  pains 
and  paresthesia.  If  it  starts  in  the  cervical  cord,  there  is  soon  a 
muscular  atrophy  of  the  hands  resembling  spinal  progressive  muscular 
atrophy,  but  with  anaesthesia.     As  the  disease  progresses  the  weakness 


326 


DISEASES    OF    THE    NERVOUS    SYSTEM 


and  atrophy  of  the  hand  muscles  become  more  noticeable  and  gradually 
extend  toward  the  trunk.  The  atrophy  often  comes  on  in  both  extremities 
at  about  the  same  time.  Fibrillary  contractions  and  partial  degeneration 
reaction  may  be  observed.  Cutaneous  anaesthesia  of  the  affected  hand 
and  arm  to  temperature  and  pain,  but  not  to  touch,  takes  place;  and 

this   is   so   marked  as   to   be   almost 
pathognomonic  of  the  disease. 

The  legs  do  not  become  affected 
until  late,  and  then  generally  show  a 
spastic  paraplegia.  The  throat  and 
face  are  rarely  involved.  There  is  a 
scoliosis  of  the  spine,  generally  in  the 
dorso-lumbar  region  (Fig.  151). 

Vasomotor,  secretory,  and  trophic 
symptoms  are  prominent.  The  hands 
may  be  oedematous  or  red  and  con- 
gested. Sweating  or  dryness  of  the 
skin  may  occur.  Eruptions  appear  on 
the  skin,  such  as  bullae,  herpes  and 
eczema.  Painless  whitlows  attack  the 
fingers  and  may  destroy  the  terminal 
phalanges.  Erosions  and  ulcerations 
also  occur.  The  nails  become  dry, 
brittle  and  drop  off.  Arthropathies 
and  spontaneous  fractures  have  been 
observed.  The  pupils  may  be  unequal 
and  the  bulb  retracted. 

Late  in  the  disease  symptoms  of  in- 
volvement of  the  medulla  develop. 
At  this  time  also  the  bladder,  rectum 
and  genital  centres  are  attacked.  The 
disease  progresses  slowly  for  years, 
with  remissions  of  various  degree. 

The  cardinal  symptoms  are  a  pro- 
gressive muscular  atrophy,  with  a  pe- 
culiar disassociated  cutaneous  anaesthe- 
sia, trophic  disturbances,  and  scoliosis. 
Pathological  Anatomy. — -The  seat  of  the  disease  is  the  substance  of 
the  cord.  On  opening  it  by  transverse  sections  one  finds  one  or  more 
cavities  extending  in  various  degrees  up  and  down.  The  most  frequent 
primary  site  is  the  cervical  swelling.  From  here  it  usually  passes  down 
and  may  reach  the  whole  length  of  the  cord.     It  also  extends  upward  and 


Fig. 


151. — Curvature    of    spine 
syringomyelia.     (Erb.) 


MUSCULAR    ATROPHIES    AND    DYSTROPHIES  327 

may  involve  the  medulla  and  the  nuclei  of  the  cranial  nerves.  The 
cavities  are  of  irregular  shape,  small  size  and  filled  with  a  liquid  like  the 
cerebrospinal  fluid.  They  are  situated  oftenest  posterior  to  the  com- 
missure and  involve  one  or  both  posterior  horns,  but  they  may  be  so  ex- 
tensive as  to  involve  almost  the  whole  of  the  centre  of  the  cord  at  some 
levels.  The  walls  are  usually  lined  by  a  membrane  and  surrounded  by 
a  gliomatous  tissue  (Figs.  153-156). 

The  glia  cells  are  in  various  stages  of  development  and  degeneration. 
In  parts  of  the  cord  the  new  growth  may  form  a  large  and  solid  mass 
occupying  most  of  the  centre  of  the  cord.  Small  hemorrhages  and  foci 
of  myelitis  may  be  present.  In  some  cases  there  is  evidence  of  a  dilated 
central  canal,  with  neuroglia  hyperplasia  of  the  walls  and  a  gliomatous 


Fig.   1o2. — Central  canal  (jf  curd  with  beginning  syringomyelia. 

infiltration  about  this.  The  epithelium  of  the  central  canal  may  form 
part  of  the  wall  of  the  cavity. 

Gliomatous  tissue  is  composed  of  small  cells,  round  or  of  irregular 
shape,  with  a  large  nucleus  and  fine  fibrillary  prolongations.  In 
glioma  these  cells  are  relatively  much  more  numerous,  while  the  fibrillary 
network  is  less  conspicuous.  When  the  fibrillary  substance  is  more 
prominent  we  have  gliosis,  and  when  it  is  almost  exclusively  fibrillary 
we  have  the  condition  found  in  multiple  sclerosis.  In  glioma  and  gliosis 
the  tissue  is  penetrated  by  small  blood-vessels  whose  walls  are  often 
diseased,  so  that  minute  hemorrhages  occur  and  the  glioma  becomes 
stained  and  pigmented.     In  other  cases  it  is  gray  or  yellowish  in  color. 

The  rich  cellular  proliferation  in  gliomata  has  suggested  an  analogy 
in  its  growth  to  that  of  inflammation,  and  the  term  gliosis  is  used  as 
analogous  for  neuroglia  to  sclerosis  of  connective  tissue.     In  gliosis  there 


328 


DISEASES    OF    THE    NERVOUS    SYSTEM 


Fig.  153. — Syringomyelia,  dorsal  segment. 

—My 


Fig.  154. — ^Total  syringomyelic  degeneration,  dorsal  segment. 


Fig.  155. — Syringomyelia,  dorsal  segment. 


Fig.  156. — Syringom3^elia,  lumbar  segment.     (From  microphofographs 
by  Dr.  C.  I.    Lambert.)  ^1 


MUSCULAR   ATROPHIES   AND   DYSTROPHIES  329 

is  a  tendency  to  softening  and  formation  of  cavities,  and  all  nerve-fibres 
disappear.  In  multiple  sclerosis  some  nerve-fibres  remain,  and  one 
observes  the  presence  of  granular  and  amyloid  bodies. 

Peculiar  Types. — 1.  The  disease  may  be  latent,  giving  rise  to  very 
few  symptoms  or  to  none  that  are  characteristic. 

2.  There  may  be  a  period  of  irritation  and  pain  in  the  extremities 
followed  by  paraplegia,  with  few  sensory  troubles,  the  course  suggesting 
a  chronic  transverse  myelitis  or  a  Brown-Sequard  paralysis. 

3.  There  is  a  type  in  which  bulbar  symptoms  develop  early,  but 
differing  from  ordinary  bulbar  paralysis  in  the  involvement  of  the 
trigeminus  and  other  cranial  nerves  not  commonly  attacked. 

4.  There  is  a  type  characterized  by  the  symptoms  of  muscular 
atrophy  with  analgesia  and  felons   (Morvan's  disease). 

Diagnosis. — The  disease  is  distinguished  in  its  classical  form  by  (1) 
its  very  slowly  progressive  course  with  periods  of  latency  and  remission; 
(2)  by  the  progressive  muscular  atrophy  combined  with  the  peculiar 
dissociated  disturbances  of  sensibility;  (3)  by  the  trophic  disturbances 
and  scoliosis. 

It  has  to  be  distinguished  from  progressive  muscular  atrophy  and 
dystrophy,  from  amyotrophic  lateral  sclerosis,  hypertrophic  cervical 
pachymeningitis,  chronic  transverse  myelitis,  Morvan's  disease  and 
anaesthetic  leprosy. 

The  sensory  and  trophic  disorders  and  scoliosis  enable  one  to  distin- 
guish it  from  progressive  muscular  atrophy.  In  leprosy  the  dissociation 
of  the  sensory  symptoms  is  not  present,  and  the  anaesthesia  is  distributed 
along  the  course  of  the  nerves  or  in  sharply  circumscribed  plaques.  In 
some  cases  the  peculiar  tubercular  disease  of  the  skin  and  the  history 
of  the  case  make  the  diagnosis  easy.  In  leprosy,  also,  there  is  a 
perineuritis,  and  the  enlarged  inflamed  nerves  may  be  felt.  Portions 
of  the  skin  may  be  excised  and  examined  for  the  leprosy  bacillus.  As 
regards  the  differentiation  from  Morvan's  disease,  this  cannot  often 
be  done.  Still  whitlows  are  rare  in  ordinary  forms  of  syringomyelia. 
Morvan's  disease  begins  in  one  hand  and  slowly  extends,  with  remis- 
sions, to  the  other.  Usually  there  is  loss  of  tactile  as  well  as  thermic  and 
pain  sense. 

The  prognosis,  so  far  as  cure  is  concerned,  is  bad;  but  the  disease 
has  often  a  long  course,  ranging  from  five  to  twenty  years,  and  periods 
occur  in  which  the  progress  of  the  disease  seems  arrested  and  improve- 
ment occurs. 

Treatment. — It  is  not  impossible  that  we  may  find  some  drug  which 
acts  specifically  on  gliomatous  tissue,  checking  its  growth.  At  present 
we  know  of  only  two  things  which  may  possibly  do  this :  nitrate  of  silver 
and  arsenic.     These  drugs  should  be  given;  and  for  the  rest,  tonic  and 


330 


DISEASES    OF    THE    NERVOUS    SYSTEM 


symptomatic  treatment  is  indicated.     Intra-spinal  medication  by  lumbar 
puncture  may  eventually  furnish  us  help  in   controlling  the  disease. 

The  use  of  radium  and  of  cross-firing 
with  X-ray  is  being  used  with  some  ap- 
parently good  result.  The  exposure  of 
the  spinal  cord  and  decompression  by 
the  method  of  Elsberg  has  been  sug- 
gested] for'gliosis.  It  has  been  success- 
ful in  isolated  gliomatous  masses.  Early 
diagnosis  and  early  attention  to  treat- 
ment are  most  important. 

THE   RECOGNITION   OF  DISEASES   OF 
THE  CAUDA  EQUINA 

Anatomy. — The  cauda  equina  is 
made  up  of  the  five  lumbar,  five  sacral 
and  one  coccygeal  nerve-roots.  They  lie 
within  the  dura  mater  forming  a  thick 
bundle  and  extending  down  the  vertebral 
canal  for  14  cm.  They  are  still  dis- 
tinct motor  and  sensory  roots,  and  do 
not  unite  till  they  have  passed  out  of 
the  dura.  The  cauda  begins  at  the 
lower  tip  of  the  cord,  at  the  level  of  the 
lower  edge  of  the  second  lumbar  verte- 
bra. The  term  conus  is  applied  to  the 
lower  end  of  the  cord  and  includes  the 
parts  below  the  second,  or  some  say 
third,  sacral  segment.  The  cord  here 
becomes  much  smaller,  loses  some  of  its 
distinctive  microscopical  structure,  and 
the  anterior  root-fibres  are  so  much 
smaller  and  less  numerous  than  the  pos- 
terior or  sensory  that  their  destruction 
causes  no  marked  paralysis. 

The  arrangement  of  the  segments  of 
the  cone  and  the  nerves  is  shown  in  Figs. 
Fig.  157.-Showing  left-half  rf  1^7  and  158.  The  arrangement  of  the 
cauda  equina,  and  tip  of  spinal  visceral  centres  is  given  by  Miiller  as 
root.  ^""'^  ^^  ^^^^^  °^  3d-lumbar    f^Hows:   second   sacral,'  erection  centre; 

third  sacral,  ejaculation  centre;  fourth 
sacral,  bladder  (detrusor)  centre ;  fifth  sacral,  sphincter  ani  centre.  The  dis- 
tribution of  the  sensory  nerves  is  shown  in  the  Figs.  127  and  128. 


MUSCULAK    ATROPHIES    AND    DYSTROPHIES 


331 


Cauda  lesions  are  generally  due  to  tumor,  pressing  on  the  part, 
neighboring  bone  disease,  and  injuries.  A  caudal  root  neuritis  has  been 
described  (Elsberg,  Kennedy),  simulating  cauda  tumor. 

The  symptoms  are  those  of  pressure  with  irritation,  and  later  de- 
struction of  the  Cauda  nerve-roots.  The  symptoms  usually  come  on 
slowly  (tumor  and  bone  disease)  with  severe  root  pains,  mostly  in  the 
sacral  nerve  distribution,  sometimes  in  the  bladder  and  rectum.     They 


Fig.  158. — Showing  arrangement  of  segments  and  nerves  of  cauda  equina. 

are  bilateral  but  more  on  one  side.  Later  and  less  notable  are  motor 
symptoms:  weakness  of  the  legs  and  loss  of  ankle  jerks.  The  sensory 
symptoms  remain  in  the  foreground.  There  is  hyper sesthesia,  then 
anaesthesia  not  symmetrical  on  the  two  sides  and  not  sharply  segmental 
as  when  the  cord  is  involved. 

Paralysis  of  the  legs  and  of  the  bladder,  sexual  and  rectal  centres 
comes  on  eventually  ?jut  usually  the  conus  is  then  also  involved. 

Cauda  lesions  must  be  differentiated  from  cord  and  especially  conus 


332 


DISEASES    OF   THE    NERVOUS    SYSTEM 


lesions  (second  to  fifth  sacral  segments) .  In  conus  lesions  we  of tener  have 
an  acute  onset  from  myelitic  softening  or  hemorrhage,  and  in  this  case 
there  is  little  pain.  Fibrillary  contractions  and  muscular  twitchings  occur. 
If  the  lesion  does  not  reach  above  the  conus  there  is  little  paralysis.  Sym- 
metrical anaesthesias  develop  in  areas  corresponding  to  the  height  of 
the  lesion  (Fig.  159),  and  there  is  sometimes  a  differentiation  of  sensibility, 


Lesion  at  second  lumbar  segment.  Lesion  at  third  lumbar  segment. 


Lesion  at  fifth  lumbar  segment. 


Lesion  at  first  sacral  segment. 


Fig.  159. — Lesions  at  different  levels  of  the  lumbar  and  sacral  cord,  showing  areas 
of  anaesthesia.     {Miiller.) 

which  does  not  occur  in  cauda  lesions.     The  bladder,  sexual  and  rectal 
centres  are  early  involved. 

In  lesions  of  the  peripheral  nerves,  the  trouble  (usually  neuritis  or 
injury)  comes  on  rather  rapidly.  There  are  sciatic  pains,  tender  points, 
the  lesion  may  be  only  unilateral,  the  pains  are  not  so  severe.  There 
is  Httle  or  no  paralysis  and  no  involvement  of  the  visceral  centres;  the 
sensory  and  motor  symptoms  go  together,  the  sensory  slightly  predom- 
inating; there  is  often  a  history  of  sciatica  and  of  alcoholism,  or  injury. 


CHAPTER  XVI 

ANATOMY  AND  PHYSIOLOGY  OF  THE  BRAIN 

Historical. — The  first  artistic  and  approximately  correct  illustra- 
tions of  the  brain  were  made  in  the  middle  of  the  sixteenth  century  (Fig. 
160.)  About  100  years  later,  the  details  became  more  accurate  (Fig.  161) 
and  in  the  next  century,  the  eighteenth  (Fig.  162),  there  is  a  modern  fine- 
ness of  finish  without  yet  absolute  accuracy,  which  was  only  acliieved  in 
the  nineteenth  century. 


Fig.  160.— The  brain.     {Vesalius,  A.  D.  1555.) 

Anatomy. — The  nervous  system  is  developed  from  a  hollow  tube  formed  by  a 
folding  of  the  epiblast.  The  brain  or  encephalon  grows  out  from  its  anterior  part. 
This  swells  into  three  cavities  called  the  anterior,  middle  and  posterior  cerebral  vesi- 
cles. From  the  anterior  a  secondary  vesicle  develops;  the  posterior  divides  into  two ; 
so  that  eventually  there  are  five  vesicles.  Out  of  them  the  different  parts  of  the  brain 
are  formed. 

333 


334 


DISEASES    OF    THE    NERVOUS    SYSTEM 


1.  From  the  anterior  vesicle  there  grow  the  cerebral  hemispheres,  the  corpus 
callosum  and  anterior  commissure,  fornix,  corpus  striatum  and  olfactory  lobes.  It 
includes  also  the  anterior  part  of  the  region  lying  under  the  thalamus  in  which 
are  the  optic  chiasm  and  pituitary  body.  These  structures  form  the  end-brain  or 
telencephalon. 

2.  From  the  posterior  part  of  the  primary  vesicle  come  the  thalamus,  pineal  gland 
(or  epithalamus),  geniculate  bodies  (or  metathalami),  and  some  structures  lying  under 
the  thalamus,  viz.,  the  corpora  mammillaria  and  Luys'  body.  These  parts  form  the 
'tween-brain  or  diencephalon. 


Fig.  161. — The  brain,  showing  the  circle  of  WiUis.     {Willis,  circ.  1665.) 

3.  From  the  middle  cerebral  vesicle  there  grow  the  corpora  quadrigemina  and 
cerebral  peduncles,  with  the  red  nuclei  and  substantia  nigra.  Thej^  form  the  mid- 
brain or  mesencephalon. 

4.  From  the  fourth  vesicle,  which  is  a  secondary  vesicle  developed  from  the  third 
primary,  come  the  "isthmus"  (which  includes  the  superior  cerebellar  peduncles  and 
valve  of  Vieussens)  and  the  "hind-brain,"  composed  of  the  cerebellum,  its  middle 
peduncles  and  the  pons.     This  part  is  also  called  the  metencephalon. 

5.  The  fifth  vesicle  (also  a  development  from  the  third)  forms  the  medulla  oblon- 
gata, or  after-brain,  or  myelencephalon. 

The  development  of  these  parts  is  shown  in  the  accompanying  Figs  163,  164. 


ANATOMY    AND    PHYSIOLOGY    OF    THE    BRAIN 


335 


The  arrangement  in  tabular  form  taken  from  Villiger's  anatomy  shows  a  slightly 
different  arrangement  as  to  the  hind-brain. 

In  man  the  fore-brain  is  enormously  developed,  the  'tween-brain  moderately 
developed,  the  olfactory  lobes  are  atrophic,  the  mid-brain  is  almost  rudimentary,  the 
hind-brain  well  developed,  the  after-brain  relatively  not  much  developed.  The 
divisions  above  given  in  detail  seem  somewhat  academic  and  impractical  as  applied 
to  adult  human  brains,  but  the  main  features  are  not  so;  indeed  they  are  quite  essential 
to  the  understanding  of  modern  anatomy. 


Fig.  162.— The  brain.     {Ruysch,  A.  D.  1724.J 


End-brain  or  telen- 
cephalon. 

'Tween-brain  or  dien- 
cephalon.  j 

Mid-brain    or    mesen-  1 


Cerebral  hemispheres,  rhinencephalon  and  corpora  striata. 
1-  Optic  thalamus  and  geniculate  bodies. 


'f  Cerebral  peduncles  and  corpora  quadrigemina. 


cephalon. 

Isthmus  and  hind-brain  1  Cerebellum  and  its  peduncles. 

or  metencephalon.       |  Pons. 

After-brain  or  myelen-  1  , .    ,   ,, 
,    .  •'  \  Medulla, 

cephalon.  j 


336 


DISEASES    OF   THE    NERVOUS    SYSTEM 


Prosencephalon — 

Fore-brain. 


Mesencephalon — 

Mid-brain. 


Rhombencephalon 

— Hind-brain. 


Telencephalon, 
End-brain. 


Diencephalon, 
'Tween-brain. 


Hemisphserium . 


[  Pallium. 

Rhinencephalon. 

Stem  of  End-brain. 

.  Pars  optica  Hypothalami. 

[  Pars  mamillaris  Hypothalami. 

[  Thalamus. 

I  Thalamencephalon.  \  Metathalamus. 

^  [  Epithalamus. 

I  Pedunculi  cerebri. 

i  Corpora  quadrigemina. 

Isthmus  rhombencephali. 

, .  ,  .    ,  I  Cerebellum. 

Metencephaion  \  „ 

.■-,,■  I  Pons, 

or  hmd-bram.  ^ 

Myelencephalon  f  - ,    ,  „      ,, 

-^      ,      .  \  Medulla  oblongata, 

aiter-bram.        [ 


M»D 


Fig.  163.  Fig.  164. 

Fig.  163. — The  cerebral  vesicles. 

Fig.  164.— Median  section  through  the  brain  of  a  human  embryo  at  the  end  of 
the  first  month.     (His.) 


In  the  process  of  development  of  the  brain,  the  neural  canal  becomes  variously 
enlarged  and  constricted,  until  the  ventricles  of  the  brain,  the  foramina  of  Monroe, 
and  the  aqueduct  of  Sylvius  are  formed.  The  ventricles  are  the  two  lateral,  the  third, 
fourth  and  fifth.  The  foramina  of  Monroe  connect  the  lateral  and  third  ventricles; 
the  aqueduct  of  Sylvius  connects  the  third  and  fourth  ventricles. 

Along  the  mesial  or  inner  surface  of  each  optic  thalamus  runs  a  groove  known  as 
the  fissure  of  Monroe.  This,  according  to  Minot,  may  be  traced  along  the  sides  of 
the  aqueduct  of  Sylvius  and  fourth  ventricle  into  the  spinal  cord,  where  it  is  identical 
with  the  line  of  division  that  in  embryonic  life  separates  the  dorsal  from  the  ventral 
parts  of  the  cord,  forming  the  dorsal  and  ventral  zones  of  His.  Minot  regards  this 
line  of  demarcation  as  having  great  morphological  importance.  All  parts  of  the  brain 
and  cord  dorsal  to  it  form  a  dorsal  zone  and  include  the  receptive  part  of  the  spinal 


ANATOMY    AND    PHYSIOLOGY    OF    THE    BRAIN  337 

cord  and  medulla,  as  well  as  of  the  cerebellum  and  cerebral  hemispheres.  This  dorsal 
zone  contains  only  nerve-cells  whose  processes  never  leave  the  nerve-centres  to  form 
nerves,  and  it  receives  all  the  entering  sensory  nerve-fibres.  It  is  the  recipient  part 
of  the  nerve-centre. 

The  ventral  zone  contains  all  cells  whose  processes  go  out  to  form  peripheral  nerves; 
it  has  also  some  cells  of  the  other  type,  but  it  does  not  receive  any  entering  sensory 
nerve-fibres.  It  is  the  efferent  part  of  the  nerve  system  and  it  includes  the  anterior 
and  part  of  the  lateral  columns  of  the  spinal  cord,  as  well  as  the  ventral  parts  of  the 
mid-,  hind-,  and  after-brains.'- 

The  different  segments  of  the  brain  are  composed  of  deposits  of  nerve  cells  forming 
gray  matter  or  ganglia,  and  of  strands  of  nerve-fibres  connecting  these  ganglia.  Most 
of  the  general  description  of  these  parts  must  be  gotten  from  treatises  on  anatomy. 

The  Cortex  Cerebri  and  the  Convolutions. — The  gray  matter  of  the  surface  of  the 
brain  is  called  the  cortex  cerebri,  and  it  is  by  far  the  largest  and  most  important 
deposit  of  nerve-cells  in  the  body.  The  cortex  is  from  2  to  4  mm.  (one-twelfth  to 
one-fifth  of  an  inch)  thick,  and  its  total  superficial  area  is  1,800  to  2,700  sq.  cm.  The 
area  of  gray  matter  lying  in  the  fissures  is  about  twice  that  lying  on  the  surface 
(Donaldson).  The  cerebral  cortex  is  arranged  in  folds  or  convolutions  (gyri)  separated 
by  fissures  or  sulci.  These  fissures  divide  the  brain  also  into  lobes.  The  fissures  of 
the  brain  are  divided  into  primary  and  secondary.  The  former  are  permanent,  and 
present  little  change  in  size,  location  or  direction.  The  latter  are  variable  in  all  these 
respects,  and  are  often  called  sulci  for  purposes  of  distinction. 

The  primary  fissures  of  the  brain  are : 

The  longitudinal. 

The  transverse  or  choroidal. 

The  fissure  of  Rolando  or  central. 

The  fissure  of  Sylvius. 

The  parietal. 

The  parieto-occipital. 

The  calcarine. 

The  position  of  these  fissures  is  indicated  in  the  accompanying  diagrams,  which 
are  based  on  descriptions  of  Eberstaller  (Figs.  167,  168,  169). 

The  primary  fissures  divide  the  cerebrum  into  various  portions  called  lobes.  The 
lobes  are; 

Frontal.  The  central  or  island  of  Reil. 

Parietal.  •  Olfactory. 

Temporal.  Limbic. 
Occipital. 

There  are  eight  fissures  and  seven  lobes.  The  position  and  arrangement  of  these 
are  indicated  in  the  illustrations. 

Microscopical  Anatomy  of  the  Convolutions. — The  cortex  of  the  cerebrum  is 
composed  of  nerve-cells,  a  network  of  nerve-fibres  and  processes,  and  of  neuroglia 
tissue.  Superimposed  upon  it  is  a  very  vascular  membrane,  the  pia  mater,  which 
sends  a  rich  plexus  of  vessels  into  it. 

The  Fibre  Layers  of  the  Cortex. — The  nerve-fibres  of  the  cortex  are  arranged  in 
more  or  less  definite  zones  or  layers.  These  layers  are  very  well  marked  in  some 
parts  of  the  cortex,  less  so  in  others.  They  have  received  different  names,  but 
adopting  the  nomenclature  and  classification  of  Campbell,  the  principal  zones  are: 

^Dr.  Adolph  Meyer  has  described  a  segmental  division  of  the  nervous  system, 
based  on  function.  Johnson  has  devised  another  scheme  of  longitudinal  division  in 
accordance  with  function.     These  are  efforts  in  a  right  direction  but  not  yet  successful. 

22 


338 


DISEASES    OF    THE    NERVOUS    SYSTEM 


1.  An  outermost  fibreless  or  neurolgia  layer. 

2.  Zonal  or  tangential  layer. 

3.  Line  of  Baillarger;  in  the  occipital  cortex  called  the  line  of  Glenari. 

4.  Radiary  zone. 

Passing  into  the  cortex  at  right  angles  to  these  layers  are  the  radiations  of  Meynert; 
and  below  the  cell  layers  are  the  association  fibres  of  Meynert. 


;i-:'.  'v.,.'>  ,.■..';  --y-'-   y-' i:h  k^ 


,1.  i 


5  I'i  : 


■  i  •   ,     •■,  .-.  ■  v. 


I 


,'  .           *•'■■,,         ■    ■        *.>■*;. 
1,..'    »■ ^     ■■  .       #.f. 


4^ 


Fig.  165. — Type  of   cell  lamination  in 
the  post-central  area.     {Camyhell.) 


Fig.  166. — Type  of  cell  lamination  in 
the  precentral  area  {Campbell).  In  the 
sixth  layer  is  seen  a  cell  of  Betz. 


Cell  Layers. — The  cells  of  the  cortex  are  also  arranged  in  layers  more  or  less  definitely 
marked,  and  varying  in  different  parts  of  the  cortex.  The  type  of  arrangement  as 
given  by  Campbell  is  as  follows : 

1.  The  plexiform  layer  containing  the  cells  of  Cajal.  It  is  also  called  the  molecular 
or  first  layer. 

2.  The  layer  of  small  pyramidal  cells;  the  cells  here  are  closely  packed,  and  while 
most  of  the  cells  are  pyramidal,  some  are  polymorphous.     This  is  called  also  the  second 


ANATOMY    AND    PHYSIOLOGY    OF    THE   BRAIN 


339 


layer.     The  cells  are  about  the  size  of  a  white  blood-cell;  this  layer  is  fused  with  the 
third  layer. 


d&pass. 


tanpM, 


Fig.  167. — ^Left  hemisphere,  from  without. 


3.  Layer  of  medium-sized  pyramidal  cells.     Here  the  cells  are  all  pyramidal  and 
increase  in  size  from  above  downward. 


f  ror\A.CLlp^i^ 


Occtpltcul-Po^- 
Fig.  168. — The  convolutions  from  above. 


4.  Layer  of  large  pyramidal  cells,  lying  on  a  level  with  the  line  of  Baillarger. 

5.  Layer  of  stellate  cells,  known  also  as  the  granule  layer  or  Kornerschicht.     This 
is  best  represented  in  the  calcarine  cortex. 


340 


DISEASES    OF    THE    NERVOUS    SYSTEM 


6.  Internal  layer  of  large  pyramidal  cells;  this  contains  the  giant  cells  of  Betz, 
and  in  the  visual  cortex  the  large  solitary  cells. 

7.  Layer  of  spindle  cells. 


Fig.  169. — Mesial  surface. 


Association,  commisural  and  projection 
fibres. 


Uncinate  fasciculus  below;  superior  longi- 
tudinal fasciculus  above. 


Fasciculus  occipito-frontalis  superior 


Cingulum    above;    inferior    longitudinal 
fasciculus  below. 

Fig.  170. — Association  tracts  of  the  brain.     (Villiger.) 


The  small  pyramidal  and  spindle  cells  measure  about  10  X  18iu;  the  large,  20  X 
40m(  K200  X^'^oo  in.).  There  are  in  the  precentral  convolutions  giant  cells  (of  Betz) 
which  measure  125  X  55/^(3-^0  0  X  }ioo  in.). 


ANATOMY  AND  PHYSIOLOGY  OF  THE  BRAIN 


341 


The  cortical  gray  matter,  as  will  thus  be  seen,  contains  layers  of  nerve-cells,  into 
which  nerve-fibres  penetrate.  These  terminate,  as  do  all  fibres,  in  end  brushes, 
which  surround  the  receptive  cells.     An  enormous  number  of  fine  fibres  is  given  off 


Fig.  171. — Vertical  section 'through  brain  immediately  behind  the  concavity  of 
the  corpus  callosum.  7,  II,  III,  Frontal  convolutions;  CC,  corpus  callosum;  V, 
lateral  ventricles;  In,  island  of  Reil;  S,  fissure  of  Sylvius;  CS,  corpus  striatum. 


by  the  cells;  some  of  these  form  layers  in  the  cortex  and  connect  neighboring  parts, 
others  run  out  and  connect  more  distant  parts  or  pass  down  to  lower  levels.  There 
are  thus  three  kinds  of  fibres — afferent,  associative  and  efferent — just  as  there  are 


Fig.  172. — Section  further  back  through  caudate  and  lenticular  nuclei,  showing  IC, 

internal  capsule. 


three  types  of  cells,  and  since  nerve-cells  and  fibres  are  really  parts  of  the  same 
unit — the  neuron — there  are  practically  three  kinds  of  neurons  in  the  cortex. 

Association  Fibres. — The  different  convolutions  and  lobes  of  the  brain  are  con- 
nected with  each  other  by  association  fibres  (Fig.  170)  and  commissural  fibres,  and 


342 


DISEASES    OF    THE    NERVOUS    SYSTEM 


Fig.  173. — Section  just  in  front  of  anterior  commissure. 


Fig.  174. — Showing  divisions  of  lenticular  nucleus.     OP,  Operculum;  //,  optic  nerves. 


*^r^   ti 


Fig.   175. — Horizontal  section  of  bram  at  level  of  the  knee  of  the  corpus  callosum, 

showing  fornix. 


ANATOMY  AND  PHYSIOLOGY  OF  THE  BRAIN 


343 


to  the  ganglionic  masses  below  them  by  projection  fibres.  The  association  fibres 
consist  of  short  fibres  connecting  neighboring  convolutions  and  of  five  long  tracts 
which  connect  neighboring  or  distant  lobes  (^Fig.  167). 

The  Central  Ganglia  of  the  Brain. — The  relations  of  the  cortex  and  of  the 
ganglionic  masses  of  the  brain  and  of  the  different  associating  tracts  is  shown  in  a 
series  of  photographs  made  by  Prof.  J.  C.  Dalton  over  twenty  years  ago.  Nothing 
so  good  has  been  done  since  his  work. 


Fig.  176. — Section  through  anterior  bend  and  splenium  of  corpus  callosum.     The 
fornix  is  nearly  removed  showing  3d-ventricle. 


Fig.   177. — Section  through   midbrain   and   cerebellum,   showing,   2,   red  nuclei,    3, 
acqueduct  of  Sylvius,  4,  pons. 

THE  CEREBELLUM 

In  man  it  consists  of  a  median  portion  or  vermis  and  two  lateral  hemispheres.  It 
is  connected  to  the  cord  and  rest  of  the  brain  by  anterior,  middle,  and  pos- 
terior peduncles.  It  is  composed  of  an  external  layer  or  cortex  of  gray  matter,  of 
central  white  matter,  and  central  ganglia.     The  gray  matter  lies  in  very  close,  nar- 


344 


DISEASES    OF    THE    NERVOUS    SYSTEM 


row  folds,  producing  with  the  white  matter  an  appearance  on  section  called  the  arbor 
vitoe.  The  vermis  and  hemispheres  are  divided  by  sulci  into  a  number  of  lobes  or 
lobules.  The  vermis  is  divided  into  superior  and  inferior  portions.  Its  further 
subdivisions  and  those  of  the  hemispheres   are  shown  in  the  cuts  (Figs.  178?and 


Central  lotule 


Mesencephalon  occupying 
th«  incisura  anterior 


Lobulus  culminis 

Lobulus  lunatus 


Postero- 
superior  lobule 


Folium  %  ermis 


Postero-inferior  lobule 


Tuber  vermis  Incisura  posterior 

Fig.  178. — Upper  surface  of  cerebellum.     {Cunningham.) 

179) .  In  the  white  matter  of  both  hemispheres  is  a  nucleus  of  small  multipolar  cells, 
the  corpus  dentatus  or  ciliary  body.  To  the  median  side  of  this,  and  belonging 
structurally  to  it,  is  a  small  nucleus,  the  emboliform  nucleus.  In  the  inferior  vermis 
is  a  collection  of  larger  multipolar  cells,  the  nucleus  fastigium  or  tegmental  nucleus; 

Central  lobule    Anterior  medullary  velam 
Brachuim  roniu^nctivuin  I  /  Ala  lobuli  centralis 

Brachium  pontis 

Fourth  ventricle-__   ,y/n  V  •^fesg^l^^S-^  ^^   ]]\^^         „        „  ,   ... 

,Tonsillacerebelli 


■Horizontal  Assure 


.Postero-inferior  lobule 


Postero-interior  lobule 


Lobulus  gracilis 

Biventral  lobule   ""   "^  7 

Pyramids 


luber  vermis 


Fig.  179. — Under  surface  of  cerebellum,  tonsil  on  right  side  removed.     {Cu7iningham.) 


just  to  the  outer  side,  between  it  and  the  emboliform  nucleus,  is  a  small  collection  of 
cells,  resembling  those  of  the  n.  fastigii,  called  the  nucleus  globosus. 

The  general  arrangement  of  the  cerebellar  cortex  is  analogous  to  that  of  the  cere- 
brum. Associative  and  receptive  cells  are  found  in  the  granular  and  molecular  layers, 
and  they  send  processes  forming  a  rich  network  around  Purkinje's  cells,  which  are 


ANATOMY  AND  PHYSIOLOGY  OF  THE  BRAIN 


345 


efferent  in  function.  The  comparatively  small  number  of  the  large  cells  is  in  harmony 
with  the  view  that  the  cerebellum  is  an  organ  that  receives  and  adjusts  nerve  impulses 
for  co-ordinate  distribution.  All  parts  of  the  cerebellar  cortex  are  anatomically  alike. 
The  white  matter  of  the  cerebellum  consists  of  nerve-fibres,  some  of  which  go  to 
form  the  peduncles.  Others  form  anterior  and  posterior  commissures,  running 
through  the  two  extremities  of  the  vermis  and  connecting  the  hemispheres.  There 
is  also  a  longitudinal  commissure  in  the  vermis.  The  white  matter  around  the  corpus 
dentatum  is  called  the  fleece. 


Fig.  180. — Transverse  section  through  a  fold  of  the  cerebellar  cortex.  P,  axon  of 
Purkinje  cell;  F,  moss  fibres;  KK',  fibres  from  white  matter  of  cerebellar  fold  ending 
in  connection  with  dendrites  of  Purkinje  cells;  M,  small  cells  of  molecular  layer; 
GR,  granule  cells;  M',  basket  cells;  GL,  neurogha  cell.     (Cunningham.) 


THE  GLANDS  OF  THE  BRAIN 


The  pituitary  body  or  hypophysis  cerebri  is  a  small  oval  body  lying  in  the  sella 
turcica  or  hypophyseal  fossa.  It  is  composed  of  an  anterior  and  a  smaller  posterior 
lobe.  It  is  connected  to  the  tuber  cinereum  above  by  a  stalk  or  infundibulum  which 
extends  downward  and  is  attached  to  the  posterior  lobe.  The  anterior  and  posterior 
lobes  are  separated  by  a  clef  t ;  and  a  narrow  strip  of  the  posterior  lobe  bordering  the 
cleft,  has  a  special  structure  which  is  called  the  pars  intermedia  (Fig.  181). 

The  anterior  lobe  is  of  ectodermic  origin,  is  glandular  in  character  and  is  developed 
from  the  primitive  buccal  cavity.  It  contains  cells  which  are  arranged  in  the  form  of 
convoluted  tubes  resting  on  a  basement  membrane.     The  blood  supply  is  rich. 

The  posterior  lobe,  like  the  anterior  is  supplied  by  a  connective-tissue  capsule 
which  sends  tuberculse  into  its  substance.     In  the  adult  it  consists  mainly  of  neuroglia 


346 


DISEASES    OF    THE    NERVOUS    SYSTEM 


with  a  few  rudimentary  ganglion  cells  and  nerve  fibers.  In  the  human  embryo  the 
nerve  elements  are  much  more  prominent. 

The  middle  lobe  or  pars  intermedia  contains  a  connective-tissue  framework  and 
epithelial  cells.  It  is  less  vascular  and  its  cells  are  smaller  than  those  of  the  anterior 
lobe.  The  pars  intermedia  contains  also  small  cyst-like  structures  which  contain  a 
colloid  substance  something  like  that  of  the  thyroid  gland. 

The  functions  of  the  pituitary  body  as  a  whole  and  of  its  different  parts,  are  de- 
scribed under  the  head  of  "Acromegaly."  Its  disease  produces  conditions  which  go 
under  the  names  of  hyper-pituitarism  and  hypo-pituitarism  and  dys-pituitarism. 
Acromegaly,  giantism,  disturbances  of  sexual  function  and  of  carbohydrate  metabo- 
lism are  among  the  disorders  attributed  to  this  organ,  destruction  of  it  not  being  com- 
patible with  life. 

The  pineal  gland  or  epiphysis  cerebri  is  a  small  organ  about  the  size  of  a  cherrystone 
placed  between  the  posterior  ends  of  the  two  thalami  and  attached  by  a  hollow  pedun- 


Foramen  inter- 
ventriculare 

Anterior  coiBmissure 

Third  ventricle 

Corpus  matnillare 

Subarachnoid  tissue 
in  cisterna  basalis 

Infundibulum 
Hypophysis 

Posterior  part  of 
subarachnoid  space 


Basilar  part  of  the 
occipital 


Sphenoidal  sinus 

Fig.  181. — Mesial  section,  showing  pituitary  gland  and  connections. 


(Cunningham. 


cle  to  the  dorsal  aspect  of  the  mesencephalon.  It  lies  quite  near  the  anterior  opening 
of  the  aqueduct  of  Sylvius,  and  its  position  is  such  that  it  is  possible  in  certain  mal- 
positions that  it  may  occlude  this  aqueduct.  It  is  a  vestigial  organ  and  is  the  repre- 
sentative of  a  median  eye  of  invertebrates,  developed  from  the  second  neuromere. 
It  has  no  special  sense  function  in  vertebrates  except  possibly  in  the  larval  forms  of 
the  very  lowest  types.  It  is  surrounded  by  a  connective  tissue  capsule  which  sends 
trabeculse  into  the  organ  dividing  it  into  small  chambers.  These  contain  tubules 
lined  with  cuboidal  epithelium  (Fig.  182).  According  to  Krabbe,  the  pineal  gland 
contains  parenchymatous  cells  which  he  terms  special  pineal  cells.  There  are  a  few 
neuroglia  cells,  but  no  nerve  fibres  except  those  that  go  with  blood-vessels. 

The  general  statement  has  been  that  this  gland  degenerates  at  the  seventh  year. 
Krabbe  has  studied  the  anatomy  of  the  pineal  gland  in  children  and  in  100  adults. 
He  finds  no  evidences  of  degeneration  in  the  gland  in  adults  and  states  that  the  struc- 
ture in  a  man  aged  ninety-two  was  similar  to  that  of  a  child  of  fourteen.  He 
describes  the  parenchymatous  cells  and  believes  them  to  be  secretory  in  function. 


ANATOMY    AND    PHYSIOLOGY    OF   THE   BRAIN 


347 


Investigations  made  by  the  writer  with  Dr.  Berkeley,  and  the  clinical  and  patho- 
logical observations  made  by  a  number  of  observers  tend  to  show  very  strongly  that 
the  gland  has  secretory  function,  having  to  do  with  the  processes  of  nutrition  and 
growth.  Its  over-activity  apparently  produces  increase  in  sexual,  mental  and  somatic 
development.     (See  "Acromegaly.") 


Non-ventricular 
part  of  thalamus 


Groove 

corresponding 

to  fornix. 

Quadrigeminal 

bodies 

Trochlear  nerve 

Brachlum 

pontis 

Brachium 

conjunctivum 

Lingula 


Medulla 
oblongata 


Genu  of  corpus 
callosum 
Corpus  callosum 
(cut) 

Cavum  septi 

■pellucidl 

Septum  pellucidum 

Caudate  nucleus 


Foramen  inter- 
ventriculare 
Anterior  commissure 
Anterior  tubercle 
of  thalamus 

Massa  intermedia 

Third  ventricle 

stria  terminalis 

Tjenia  thalami 

Trigonum  habenulae 

Posterior 

commissure 

Stalk  of  pineal  body. 

Pulvinar 


Pineal  body 


Fig.  182. — Showing  pineal  gland,  and  basal  ganglia. 


THE  CONNECTING  TRACTS  OF  THE  BRAIN 

The  white  matter  of  the  brain,  as  abeady  shown,  is  made  up  of: 
[  Short. 

1.  Association  fibres       {  Long. 

[  Commissural. 

2.  Projection  fibres  and  interganglionic  tracts. 

1.  The  association  fibres  of  the  cortex  have  been  already  described. 

2.  The  projection  fibres  are  those  which  connect  different  areas  of  the  cortex  with 
the  basal  ganglia  and  the  ganglionic  masses  of  the  pons,  medulla  and  spinal  cord. 

The  projection  fibres  of  the  brain  form  the  different  pathways  (a)  by  which  the 
special  and  general  sensations  pass  up  to  the  brain  cortex  and  (b)  by  which  the  volun- 
tary, automatic,  and  psycho-reflex  movements  of  the  body  are  brought  about. 

The  Efferent  Tracts. — The  cerebrospinal  efferent  paths  are  of  two  kinds:  The 
direct  or  voluntary  and  the  indirect  or  extra-pyramidal  tracts. 

The  direct  motor  or  upper  motor  neuron  tract  originates  from  cells  in  the  precentral 


348 


DISEASES    OF   THE    NERVOUS    SYSTEM 


convolutions;  the  neuraxons  of  these  cells  pass  down  and  are  gathered  together  in  a 
narrow  band  which  passes  through  and  occupies  the  anterior  two-thirds  of  the  poste- 
rior segment  of  the  internal  capsule.  The  fibres  continue  on  into  the  pons  Varolii 
and  medulla,  and  at  the  latter  point  give  off  some  terminals  which  cross  (except  those 
for  the  sixth  nerve)  to  the  nuclei  of  the  motor  cranial  nerves.  The  rest  of  the  bundle 
passes  on  through  the  medulla,  and  90  per  cent,  cross  over  at  its  lower  portion, 


Crura  Cerebri 


'<^/^^/i 


Medul+s 


Spinal  Cord 


Spinal  Cord 


Spinal  Cord 


Fig.  183.  Fig.  184. 

Fig.  183.^ — Showing    the  course  of  the  pyramidal   (cortico-bulbo-spinal    motor) 
tract.     Showing  the  upper  and  the  beginning  lower  motor  neurons. 
Fig.  184.- — -Diagram  of  the  indirect  motor  tract. 


forming  there  the  anterior  pyramids.  About  10  per  cent,  of  the  fibres  do  not  cross, 
however,  but  continue  on  the  same  side.  The  crossed  bundle  passes  into  the  lateral 
column  of  the  spinal  cord,  forming  the  crossed  pyramidal  tract,  which  passes  on,  dimin- 
ishing in  size  as  far  as  the  sacral  part  of  the  cord.  It  gives  off  terminal  end  brushes 
which  surround  the  cells  of  the  anterior  horns.  The  small  uncrossed  band  of  fibres 
continues  on  in  the  mesial  part  of  the  anterior  column,  forming  the  direct  pyramidal 
tract,  or  column  of  Ttirck.     The  fibres  of  this  tract  cross  over  in  the  anterior  commis- 


ANATOMY    AND    PHYSIOLOGY    OF    THE    BRAIN  349 

sure  at  different  levels,  and  their  teminals  also  connect  with  the  motor  cells  of  the 
anterior  horns.  From  these  horns  the  lower  motor  neuron  passes  out  to  the  muscles. 
Hence  the  voluntary  motor  system  is  a  two  neuron  mechanism. 

Each  tract  as  it  reaches  the  spinal  cord  contains  about  80,000  fibres. 

The  indirect  efferent  tract  {long  extra-pyramidal  tracts)  arises  from  nerve-cells  in 
the  anterior  central  convolution  and,  to  some  extent  in  the  frontal  lobe  adjoining. 
Its  fibres  pass  down  into  the  internal  capsule,  mingling  directly  with  those  of  the  direct 
motor  tract  and  giving  off  collaterals  to  the  optic  thalamus.  The  fibres  pass  through 
the  cerebral  peduncles,  occupying  their  inner  four-fifths,  or  motor  part,  and,  finally, 
reach  certain  deposits  of  nerve-cells  in  the  pons  Varolii  known  as  the  pons  nuclei. 
They  surround  these  cells  here  with  terminal  end  brushes.  From  these  cells  neuraxons 
cross  the  median  line  in  the  middle  cerebellar  peduncle  and  thence  to  the  cortex  of 
the  lateral  lobes  of  the  cerebellum,  where  they  in  turn  end.  From  here  the  nerve- 
cells  send  fibres  to  the  nuclei  of  the  cerebellum  and  Deiter's  nucleus,  thence  down  into 
the  spinal  cord,  where  they  pass  along  mainly  in  the  lateral  fundamental  columns,  to 
connect  finally  with  the  anterior-horn  cells.  Other  fibres  from  the  cerebellar  cortex 
pass  to  the  dental  nuclei,  then  cross  to  the  red  nuclei.  Then  some  fibres  pass  spinal- 
ward  in  the  lateral  columns  to  the  anterior  horns.  Thus  it  will  be  seen  that  the  in- 
direct motor  tract  is  composed  of  (a)  a  cortico-pontile  neuron,  (&)  a  pons-cerebellar 
neuron,  (c)  a  cerebello-nuclear  neuron,  {d)  nuclear-rubro-spinal  and  nuclear-Deiter- 
spinal,  and  (e)  the  peripheral  motor  neuron. 

The  short  extra-pyramidal  tracts  have  been  described  (see  p.  202),  but  they  may 
all  be  grouped  together  here.  They  all  end  in  the  cells  of  the  anterior  or  lateral 
horns  of  the  cord. 


SUMMARY:  EFFERENT  TRACTS  FROM  BRAIN  TO  CORD 


2  Neuron  system  from         I.  Pyramidal    tract:    (1)   cortex  of  anterior  central  con- 
cerebellum,  volution.     (2)  Spinal  cord  to  muscle. 
2  Neuron  system  from        II.  Short  extra-pyramidal  tracts. 
mid-brain.  A.  Tecto-spinal  tract :  (1)  corpora-quadrigemina  cross- 
ing to  anterior  horn  cells,  (2)  to  muscle. 
2  Neuron  system  from  B.   Fasciculo-spinal  tract:  (1)  Cajal's  nucleus  in  pos- 
mid-brain.  terior  longitudinal  bundle,  uncrossed  to  anterior 

column,  to  anterior  horn  cells,  (2)  to  muscle. 
2  Neuron  system  from  C.  Rubro-spinal   tract:  (1)    Red   nucleus,  crossing  to 

mid-brain.  antero-lateral  tract,  to  anterior  horn  cells,   (2)  to 

muscle. 

2  Neuron  system  from  D.  Vestibulo-spinal  tract :  (1)  Deiter's  nucleus  crossing 
after-brain.  in  part  to  peripheral  part  of  antero-lateral  column 

3  Neuron  system  from  to  anterior  horn  cells,  (2)  to  muscle, 
vestibular  nerve. 

4,  5,  or  6  Neuron  sys-  III.  Long  extra-pyramidal  tract:     Cortico-pontile;  pons- 

tem .  cerebellar ;  cerebellar-nuclear ;  nuclear-Deiter; 

Deiter-spinal;  anterior  horn  cells  to  muscles. 


The  direct  or  pyramidal  tracts  are  all  concerned  with  voluntary  motion  and  in- 
hibition, and  when  the  anterior-horn  cells  of  the  cord  are  cut  off  by  a  lesion  of  these 


350 


DISEASES    OF    THE    NERVOUS    SYSTEM 


tracts  there  is  a  spastic  or  upper  neuron  type  of  paralysis.  The  indirect  and  extra- 
pyramidal motor  tracts  are  concerned  in  the  co-ordination  of  bodily  movement  and 
in  securing  muscular  tonus  and  synergy  and  in  the  higher  reflex  automatic  acts.  The 
course  of  the  direct  and  indirect  motor  tracts  is  shown  in  the  accompanying  diagrams 
(Figs.  183,  184). 

The  Afferent  Tracts. — The  next  important  pathways  in  the  brain  and  cord  are 
the  sensory,  and  they  are  concerned  in  bringing  tactile,  muscular  and  general  sensa- 
tions from  the  remoter  parts  of  the  body  to  the  cortex  of  the  brain.     It  will  be  easier 


Crura  Cerebri 


Pons 


Pons 


Medulla 


PosTeriorRooT- 

Spinal  Cord 
Fig.  185. — The  afferent  tract  (3  neurons)  for  pain  and  temperature. 


to  follow  these  tracts  if  we  begin  at  the  periphery  and  follow  the  course  of  the  fibres 
up  to  their  centres  in  the  brain. 

The  Cutaneous  Sensory  Tract. — A  tactile  irritation  of  the  skin  passes  up  the  sen- 
sory nerve  to  a  posterior  spinal  ganglion,  where  the  cell  body  from  which  the  fibre  is 
derived  is  found.  It  passes  directly  through  the  gangUon,  enters  the  posterior  root 
of  the  spinal  cord,  and  passes  up  to  a  group  of  cells  lying  in  the  posterior  horns,  where 
it  meets  and  surrounds  with  its  end  brush  a  second  sensory  cell.  A  second  neuraxon 
starts  from  the  body  of  this  cell;  most  fibres  cross  over  in  the  posterior  commissures 


ANATOMY    AND    PHYSIOLOGY    OF    THE   BRAIN  351 

of  the  spinal  cord  to  the  posterior  column  of  the  other  side  where  they  run  up  in  the 
posterior  columns  and  gray  matter  (probably  in  chains  of  successive  neurons),  reach 
the  medulla  and  pons,  and  pass  through  this  to  the  optic  thalamus.  Here  they  send 
terminals  to  another  cell,  which  in  turn  sends  a  neuraxon  to  the  cortex  of  the  post- 
central convolutions.  Thus  the  cortical  centres  of  the  direct  sensory  path  are  just 
posterior  to  the  area  from  which  the  motor  tract  started.  The  direct  tactile  tract  is 
made  up  of  (1)  a  peripheral  sensory  neuron,  (2)  a  series  of  intrasiiinal  neurons,  (3)  a 
spinal-thalamic  neuron,  (4)  a  thalamic-cortical  neuron 

The  pain  and  temperature  fibres  take  a  similar  course  except  that  they  cross  over 
in  the  anterior  commissure,  do  not  run  in  chains  of  neurons  and  ascend  in  the  lateral 
columns  to  the  thalamus  (Fig.  185). 

The  deep  sensory  tracts  convey  impulses  which  originate  in  muscles,  joints  and  the 
viscera.  The  impulses  pass  up  sensory  nerves  through  the  posterior  roots.  Some 
now  pass  directly  into  the  posterior  column  of  the  cord  of  the  same  side  and  ascend 
till  they  reach  the  upper  end,  where  their  end  brushes  surround  the  cells  of  the  nuclei 
of  the  column  of  GoU  and  of  Burdach.  From  there  they  cross  to  the  other  side  in  the 
sensory  decussation.  Some  then  go  to  the  red  nuclei  and  optic  thalamus,  where  they 
terminate.  Another  neuron  now  carries  the  impulse  on  to  the  parietal  convolutions . 
Another  set  of  deep  afferent  impulses  goes  from  the  sensory  roots  to  the  cells  of  the  col- 
umn of  Clark,  thence  by  the  cerebellar  tracts  to  the  cerebellum.  This  indirect  afferent 
tract  is  thus  composed  of  (1)  a  peripheral  sensory  neuron,  (2)  a  spinal-cerebellar  neu- 
ron, (3)  a  cerebellar-thalamic,  and  (4)  a  thalamic-cortex  neuron.  Here,  too,  the 
mechanism  is  not  so  simple.  Some  of  the  afferent  fibres  do  not  go  higher  than  the 
cerebellum,  but  are  reflected  to  lower  nuclei  of  the  brain  stem  and  thus  automatic 
movements  and  the  higher  reflexes  are  brought  about.  The  direct  sensory  tracts 
carry,  for  the  most  part,  the  sense  of  touch,  pain,  and  temperature.  Some  direct 
sensory  tracts  are  concerned  with  the  sensation  from  the  muscles  and  joints  which 
have  to  do  with  co-ordination,  and  also  with  visceral  sensations.  It  is  through  the 
indirect  sensory  and  indirect  motor  tracts  that  the  automatic  and  psycho-reflex  acts 
are  performed. 

SUMMARY:  AFFERENT  TRACTS  FROM  SPINAL  CORD  TO  BRAIN 

3  Neuron  system.  I.   (1)  Posterior  gangUon  cell  to  posterior  column  and 

Deep  sensibility.  nuclei  of  columns  of  Goll  and  Burdach,  (2)  cross- 

ing in  medulla  to  optic  thalamus,  (3)  to  cortex  of 
parietal  lobe. 

3  Neuron  system.  II.  (1)  Posterior  ganglion  cell  to  posterior  horn,  (2) 
Pain  and  temperature.  crossing  to  antero-lateral  column  to  thalamus,  (3) 

to  cortex  of  parietal  lobe. 

4  Neuron  system.  III.  (1)  Posterior  ganglion  cell  to  posterior  horn,  (2) 
Tactile  sensation.  partly  crossing  to  chains  of  neurons  in  gray  matter, 

(3)  posterior  and  lateral  columns  to  thalamus,  (4) 
to  cortex  of  parietal  lobe. 

2  Neuron  system.  IV.  (1)  Posterior  ganglion  to  cells  of  Clark's  columns,  (2) 
Equilibrium,  etc.  uncrossed  to  direct  cerebellar  tract  to  cortex  of 

vermis  of  cerebellum. 

3  Neuron  system.  V.  (1)  Posterior  ganglion  to  cells  of  intermediate  gray 
Equilibrium,  etc.  matter  of   cord,    (2)   partly   crossing  to  ventral 

cerebellar  (Gowers')  tract,    (3)  to  anterior  cere- 
bellar peduncles  to  vermis. 


352  DISEASES    OF    THE    NERVOUS    SYSTEM 

Other  Projection  Systems. — The  optic,  acoustic,  and  olfactory  projection  tracts 
are  described  in  connection  with  their  peripheral  nerves  or  end  organs. 

THE  MEMBRANES  OF  THE  BRAIN 

The  membranes  of  the  brain  are  the  dura  mater,  the  arachnoid,  and  pia  mater. 
The  dura  mater  lines  the  inner  surface  of  the  skull.  It  is  attached  loosely  to  the 
concavity,  but  closely  to  the  base.  It  splits  into  two  layers  to  form  the  venous 
sinuses  of  the  skull.  The  inner  of  the  two  layers  at  certain  points  projects  inward  to 
form  membranous  septa.  These  are  known  as  the  great  longitudinal  or  cerebral 
falx,  the  lesser  longitudinal  or  cerebellar  falx,  and  the  tentorium.  Hence  both 
venous  sinuses  and  membranous  septa  are  formed  out  of  the  inner  layer.  The 
outer  layer  forms  the  periosteum  of  the  bone.  The  dura  mater  is  supplied  with 
sensory  nerves,  chiefly  by  the  trigeminus  but  posteriorly  by  the  vagus.  The  blood- 
supply  wUl  be  described  later. 

The  arachnoid  is  a  thin,  transparent,  fibrous,  non-vascular  membrane  lying  be- 
tween the  pia  and  dura  and  continuous  with  the  spinal  arachnoid.  It  bridges  over 
the  fissures  and  the  depressions  at  the  base  of  the  brain  and  forms  between  the  pia  and 
itself  certain  lacunae  or  cisterns.  These  are  the  central  lacuna  found  at  the  beginning 
of  the  fissure  of  Sylvius,  the  callosal,  those  of  the  transverse  fissures  and  of  the 
lateral  aspect  of  the  pons  Varolii.  The  space  between  the  dura  and  arachnoid  is 
called  the  subdural  or  arachnoid  cavity.  It  is  lined  with  epithelium  and  resembles 
other  serous  cavities.  The  inner  surface  of  the  arachnoid  is  connected  with  the  pia  by 
numerous  delicate  fibrous  processes.  The  space  between  these  membranes  is  called 
the  subarachnoid  space.  It  communicates  with  the  subdural  space  by  means  of  the 
foramen  of  Magendie,  which  lies  in  the  part  of  the  arachnoid  that  passes  over  the  pons 
and  medulla,  closing  in  the  fourth  ventricle;  also  by  means  of  the  lateral  recesses  of 
the  fourth  ventricle. 

The  subdural  and  subarachnoid  spaces  contain  a  serous  fluid.  It  is  called  the 
cerebro-spinal  fluid,  and  comes  mostly  from  the  choroid  plexus  of  the  lateral  ven- 
tricles. The  arachnoid  contains  no  nerves  or  blood-vessels.  It  is  described  by  some 
as  a  part  of  the  pia  mater. 

The  pia  mater  lies  beneath  the  arachnoid  and  is  closely  applied  to  the  brain  in  all 
its  folds.  It  is  continuous  with  the  spinal  pia.  It  is  very  vascular  and  supplies  the 
whole  periphery  and  part  of  the  interior  of  the  brain  with  blood.  It  consists  of  two 
layers:  an  outer  holding  the  larger  vessels,  and  an  inner  delicate  layer  closely  asso- 
ciated with  the  superflcial  neuroglia  of  the  brain.  The  pia  mater  folds  upon  itself 
and  passes  through  the  transverse  fissure  into  the  third  and  lateral  ventricles  of  the 
brain.  These  vascular  folds  form  the  velum  interpositum,  which  gives  off  a  choroid 
plexus  to  the  lateral  and  third  ventricles.  Another  fold,  the  inferior  choroid  plexus,  is 
given  off  to  the  fourth  ventricle.     The  pia  mater  has  vasomotor,  but  no  sensory  nerves. 

Functions  of  the  Brain  Membrane. — The  dura  mater,  by  its  outer  layer,  acts  as  a 
periosteum;  by  its  inner  layer  as  a  lymph  sac.  It  is  also,  by  virtue  of  its  sensitiveness, 
a  protection  against  injury  and  disease.  It  is  supplied  with  sensory  nerves,  but  is 
not,  in  fact,  very  sensitive  normally  and  may  be  cut  and  handled  without  pain. 
Strains  upon  it,  however,  do  cause  some  pain  (Gushing).  The  arachnoid  forms  the 
inner  wall  of  the  sac.  The  pia  mater  is  a  vascular  and  nutritive  organ.  It  is,  however, 
also  closely  connected  with  the  lymphatic  system  of  the  arachnoid.  The  blood  and 
cerebrospinal  fluid  of  the  brain  vary  in  amount.  In  congestion  the  cerebrospinal  fluid 
can  pass  into  the  spinal  subarachnoid  cavity  or  be  rapidly  taken  up  by  the  absorbents. 
In  anaemia  and  atrophy  there  may  be  compensatory  increase  of  the  fluid. 

The  cerebrospinal  fluid  is  a  secretion  and  comes  mostly  from  the  choroid  plexuses 


ANATOMY    AND    PHYSIOLOGY    OF    THE   BRAIN  353 

of  the  lateral  ventricles  which  are  covered  by  the  ependyma.  These  can,  if  needed, 
pour  out  an  enormous  amount  which  flows  into  the  third  and  fourth  ventricles  and 
thence  through  the  foramina  of  Magendie  and  Luschka  into  the  subarachnoid  cavities 
of  the  brain  and  cord.  It  flows  under  a  pressure  of  5  to  20  mm.  of  mercury  and  is 
eventually  absorbed  by  the  blood-vessels  (veins  and  sinuses  of  the  brain).  A  little 
of  it  probably  leaks  into  the  cavity  of  the  arachnoid  proper.  The  cerebrospinal 
fluid  is  colorless,  transparent,  alkaline.     Specific  gravity,  1,007. 

Its  composition  is  about  as  follows  (Halliburton) :  water  99,  solids,  1.  The  solids 
consist  of:  Pi'oteids,  0.085;  extractives,  0.060;  salts,  0.865. 

The  proteids  consist  of  serum  globulin,  and  allied  bodies.  (Albumin  is  a  normal 
ingredient,  according  to  Bernstein.)  A  substance  that  reduces  Fehling'  solution  is 
present.  There  is  no  fibrin  ferment,  and  the  fluid  does  not  coagulate  on  boiling,  or 
there  is  only  a  trace  of  turbidity.  Under  the  microscope  it  is  practically  free  from 
cellular  bodies.  The  normal  amount  of  fluid  ranges  from  5ii-  to  §ii.,  being  greater 
in  the  aged. 

There  occur  changes  in  the  spinal  fluid  in  inflammatory  and  degenerative  diseases 
of  the  spinal  cord,  including  syphilis,  tumors  of  the  cord  and  brain,  and  herpes  zoster. 
The  Blood-supply  of  the  Brain  and  its  Membranes. — The  vascular  supply  of  the 
scalp,  skull,  and  dura  mater  comes  from  the  external  carotids;  that  of  the  eye,  brain, 
and  pia  mater  from  the  internal  carotids  and  vertebrals.  The  arrangement  is  shown 
here: 

Occipital,  inferior  meningeal,  arteries. 
Posterior  auricular. 
[  Anterior. 
<   Temporal  \  Middle. 
[  Posterior. 
Ascending  pharyngeal,  posterior  meningeal. 
Internal  maxillary,  middle  meningeal,  small  meningeal. 
Anterior  meningeal. 
Anterior  cerebral. 
Middle  cerebral. 
Posterior  communicating. 
Anterior  choroid. 
J  Posterior  meningeal. 
\  Inferior  cerebellar. 
Anterior  cerebellar. 
Superior  cerebellar. 
Posterior  cerebral. 


External  carotid 
gives  off 


Internal  carotid 
gives  off 


Vertebral      and 
basilar  give  off 


The  blood-supply  of  the  meninges  comes  from  the  anterior,  middle,  and  posterior 
meningeal  arteries.  These  all  come,  except  the  small  anterior  meningeal  branches 
and  a  small  posterior  branch,  from  the  external  carotid.  The  blood  passes  into  the 
diploic  veins,  and  from  there  passes  chiefly  into  the  lower  occipital  and  lateral  sinuses . 
Some  of  it,  however,  returns  in  the  venae  comites.  It  all  returns  down  toward  the 
base  of  the  skull.  The  most  important  of  the  arteries  is  the  middle  meningeal,  both 
on  account  of  its  size  and  its  distribution  above  important  functional  areas. 

The  blood-supply  to  the  pia  mater  and  brain  substance  comes  from  the  internal 
carotid  and  the  vertebral  arteries.  The  branches  of  the  former  artery  give  off  the 
anterior  and  middle  cerebral,  the  posterior  communicating  and  anterior  choroid. 
The  vertebral  arteries  give  off  the  inferior  cerebellar,  while  the  basilar  branch  of  the 
vertebrals  gives  off  the  transverse,  anterior  cerebellar,  superior  cerebellar,  and  pos- 
terior cerebral  arteries. 
23 


354 


DISEASES    OF    THE    NERVOUS    SYSTEM 


The  anterior,  middle  and  posterior  cerebral  arteries,  are  the  three  largest  and  most 
important.  By  their  anastomoses  the  circle  of  Willis  is  formed  (Fig.  161).  From 
the  circle  of  Willis  and  the  beginnings  of  the  three  arteries  mentioned,  several  groups 
of  vessels,  six  in  all,  are  given  off.  They  enter  the  base  of  the  brain  and  supply  the 
great  basal  ganglia  and  adjacent  white  matter.  They  are  called  the  central  arteries; 
they  do  not  anastomose,  and  they  are  the  vessels  usually  affected  in  cerebral  hemor- 
rhages of  adult  life.  One  set  of  these  central  arteries,  the  internal  striate,  passes  up 
and  supplies  the  two  inner  segments  of  the  lenticular  nucleus,  the  caudate  nucleus  and 
anterior  part  of  the  internal  capsule.  Another  set,  the  external  striate,  divide  into  an- 
terior or  lenticulo-striate  branches  which  supply  the  lenticular  nucleus  and  posterior 


Anterior  meningeal 

artery 
Anterfor  branch  of 
middle  meningeal 
artery 

Deep  temporal 
arteries 

Infra-orbital 

artery 

Middle  menin- 
geal artery 


Accessory 

meningeal 

artery 


Posterior  superior 
alveolar  artery 


•Bucciijator  artery 


Mental  artery 


Submental  artery 


Posterior  branch 
of  middle  men- 
ingeal artery 
Superficial  tern-, 
poral  artery 

Internal  maxil 
lary  artery 

Occipital  artery' 

Inferior  alveolar 
arteiy 

Mylo-hyoid  artery 
Posterior  auricular 
artery 

Sterno-mastoid  muscle 

levator  scapul3e_ 

muscle 

Trapezius  muscle  - 

Occipital  artery- 
External  carotid  artery- 
External  maxiUary  artery- 
Lingual  artery- 
Internal  carotid  artery 
Scalenus  medius  muscle ' 

Superior  thyreoid  artery 

Common  carotid  artery 

Fig.  186. — The   external   carotid,   internal  maxillary   and  meningeal  arteries. 

(Cunningham.) 

part  of  the  caudate.  One  of  these  larger  than  the  rest  is  called  the  artery  of  cerebral 
hemorrhage.  The  other  or  posterior  branch  is  called  the  lenticulo-optic  and  supplies 
the  anterior  part  of  the  thalamus.  According  to  Kalisko,  the  lenticular  nucleus  is 
supplied  in  part  by  a  branch  from  the  anterior  cerebral.  This  he  calls  the  artery  of 
cerebral  thrombosis.     It  is  especially  effected  in  severe  gas  poisoning. 

The  cortical  arteries  are  the  terminal  branches  of  the  great  cerebral  arteries.  They 
anastomose  with  each  other  but  shghtly  They  are  distributed  very  widely  and 
carry  much  more  blood  than  tLe  central  groups.  Their  distribution  is  shown  in  Figs. 
18/ ,  1 68.  The  cortical  arteries  are  distributed  in  the  pia,  and  from  there  they  pass 
in  two  sets,  a  superficial  and  a  deep,  into  the  gray  matter,  and  for  a  short  distance 
into  the  white  matter.     They  pass  straight  in  at  right  angles  to  the  surface.     They 


ANATOMY  AND  PHYSIOLOGY  OF  THE  BRAIN 


355 


have  richly  arborescent  branches  which  do  not  anastomose;  consequently  a  knife 
plunged  straight  into  the  brain  does  not  cut  many  vessels. 

The  capillaries  are  surrounded  by  spaces  called  perivascular  spaces  which  serve 
as  lymphatic  channels.  The  neuroglia  cells  send  processes  which  connect  with  or 
form  passages  to  the  vessel  walls. 


Fig.  187. — Distribution  of  arteries  on  convexity  of  cerebrum.     Middle  cerebral  in 
black-;  anterior  cerebral  in  gray;  posterior  cerebral  in  white. 


Fig.  188. — Arteries  of  mesial  and  inferior  surface  of  cerebral,  in  black,  gray  and  white 

as  in  previous  figure. 

NoTE.^ — The  caudate  nucleus  is  supplied  by  the  anterior  and  middle  cerebral 
central  arteries. 

The  lenticular  nucleus  by  the  anterior  choroid  (part  of  its  internal  and  external 
segments),  by  the  anterior  cerebral  (caudate  nucleus  and  external  and  middle  seg- 
ments of  lenticular),  by  the  middle  cerebral  (caudate  nucleus  and  middle  and  external 
segments  of  lenticular). 

The  optic  thalamus  by  the  posterior  communicating  anterior  choroid  (external 
nucleus)  and  the  posterior  cerebral.     (Fig.  209,  p.  434.) 


356 


DISEASES    OF    THE    NERVOUS    SYSTEM 


The  corpora  quadrigemina  and  geniculate  bodies  are  supplied  by  the  posterior 
cerebral. 

The  red  nucleus  by  the  posterior  cerebral,  and  the  subthalamic  region  by  the  pos- 
terior communicating. 

The  internal  capsule  by  the  anterior  cerebral  and  middle  cerebral  for  its  anterior 
part,  by  the  posterior  communicating,  anterior  choroid  and  the  middle  cerebral  for  its 
posterior  part.  None  of  the  thalamus  is  supplied  by  the  middle  cerebral  and  none  of 
the  internal  capsule  by  the  posterior  cerebral.  All  direct  thalamus  lesions  must  be 
posterior  cerebral,  or  in  minor  degree  posterior  communicating.  No  direct  capsular 
lesions  would  come  from  the  posterior  cerebral  (Beevor).  (See,  however.  Fig.  209, 
Bing.) 

The  cortical  areas  of  the  brain  supplied  by  the  anterior,  middle  and  posterior  vary 
somewhat;  the  three  chief  systems  anastomose  at  the  parts  where  one  region  joins  the 
other  (Duret,  Beevor).  The  cortical  arteries  do  not  anastomose  with  the  central  or 
ganglionic  arteries  which  latter  supply  the  centrum  ovale. 


Foramenparietale 


I'teuis  reriedra/is 


^^    VmajiufiUarts  externa 

Fig.  189. — ^The  cerebral  sinuses.     {Hermann.) 


The  blood  of  the  convex  and  mesial  cerebral  surface,  flowing  up  from  the  base, 
leaves  the  capillaries  and  enters  veins.  Thence  it  still  passes  upward,  and  for  the 
most  part  enters  the  longitudinal  sinus.  The  most  of  the  vessels  enter  the  posterior 
portion  of  the  sinus  and  in  a  direction  forward  and  upward;  i.e.,  against  the  current 
in  the  sinus.  The  course  of  the  blood-current  is,  therefore,  opposed  both  to  gravita- 
tion and  to  the  venous  flow. 

The  veins  of  the  cerebrum  are:  1,  the  superficial  cerebral;  2,  the  deep  cerebral 
and,  3,  the  cerebral  sinuses.  1.  The  superficial  cerebral  veins  are  venae  comites. 
Those  on  the  convex  and  mesial  surfaces  empty  chiefly  into  the  superior  longitudinal 
sinus,  as  described;  those  on  the  basal  surface  and  temporal  lobes  empty  into  the 
cavernous  and  lateral  sinuses.  These  veins  have  no  valves,  and  their  walls  are  very 
thin  and  without  muscular  fibres.  2.  The  deep  cerebral  veins,  or  venae  Galeni, 
receive  the  blood  from  the  lateral  ventricles  and  from  some  of  the  central  arteries 


ANATOMY  AND  PHYSIOLOGY  OP  THE  BRAIN 


357 


supplying  the  basal  ganglia.  They  empty  into  the  straight  sinus.  These  deep  or 
central  veins  when  compressed  lead  to  stasis  and  internal  hydrocephalus.  3.  The 
cerebral  sinuses  are  fifteen  in  number.  The  important  ones  are  the  superior  and  in- 
ferior longitudinal,  the  straight,  the  lateral,  the  occipital,  the  cavernous,  and  the 
superior  and  inferior  petrosal.  They  carry  blood  for  the  most  part  in  a  direction 
from  before  backward,  and  convey  it  eventually  to  the  internal  jugular  (Fig.  189). 

Most  of  the  blood  of  the  convexity  and  mesial  surface  must  pass  into  the  longitu- 
dinal sinus,  but  there  is  a  slight  connection  of  some  of  the  veins  with  the  superior 
petrosal  and  straight  sinuses.  The  superior  longitudinal  sinus  also  communicates 
slightly  with  veins  of  the  scalp  and  with  the  facial  vein.  Some  of  the  blood  from  the 
mesial  surface  also  goes  to  the  veins  of  Galen. 

On  the  whole,  however,  the  system  of  the  convex  and  mesial  cerebral  surface  is  a 
close  corporation,  the  blood  having  to  pass  into  the  superior  longitudinal  sinus  and 


Fig.  190. — Localization"  of  functions  of  the  cortex  of  the  brain.     Median  surface. 


torcular  Herophili,  where  it  meets  that  of  the  straight  and  occipital  sinuses,  and  flows 
forward  through  the  lateral  sinuses  to  the  internal  jugular.  The  circulation  of  the  basal 
surface  is  less  isolated.  All  the  basal  sinuses  communicate  with  each  other  freely,  and 
there  are  slight  communications  between  the  veins  of  the  scalp  and  the  cavernous, 
lateral,  and  inferior  petrosal  sinuses.  It  is  safe  to  tie  any  of  the  sinuses,  except  the 
lateral  and  the  posterior  part  of  the  longitudinal.  The  cerebellar  veins,  superior, 
inferior,  and  lateral,  empty  into  the  straight,  the  lateral,  and  superior  petrosal  sinuses. 
None  of  the  cerebral  veins  or  sinuses  have  valves. 

The  pressure  of  the  blood  as  it  goes  through  the  external  carotid  is  about  150  to 
200  mm.  of  mercury.  The  pressure  of  the  blood  in  the  cranial  cavity  is  much  less 
(from  0  to  50  mm.  of  Hgr.,  Hill).  The  pressure  in  the  central  arteries  is  greater  than 
that  of  the  cortical.  The  pressure  of  the  venous  blood  is  very  slight  and  is  ordinarily 
the  same  as  that  of  the  cerebrospinal  fluid. 

Both  arteries  and  veins  are  more  delicate  than  the  extra-cerebral  vessels. 

Except  in  gray  matter,  the  brain  is  not  a  very  vascular  organ,  but  this  gray  tissue 


358 


DISEASES    OF    THE    NERVOUS    SYSTEM 


ranks  in  richness  of  blood-supply  with  the  lungs  and  liver.  The  amount  of  blood  in 
the  brain  at  any  one  time  is  only  about  1  to  2  per  cent,  of  the  total  blood  in  the  cir- 
culation, or  about  four  ounces  (Ranke). 

THE  FUNCTIONS  OF  THE  BRAIN 

Cerebral  Localization. — -The  brain  is  the  seat  of  conscious  intelligence  and  other 
psychic  activities.  It  exerts  control  and  direction  over  voluntary  movements,  it  is 
the  seat  of  instinctive  acts,  and  it  regulates  in  a  measure  the  vaso-motor,  trophic, 
and  secretory  mechanisms  of  the  body. 

The  Prefrontal  Lobes. — ^The  prefrontal  lobes,  or  that  part  of  them  which  is  in 
front  of  the  precentral  convolution,  are  concerned  with  the  higher  association  processes 
and  memories.  The  most  anterior  portion,  according  to  Campbell,  though  of  late 
development  is  poor  in  cortical  cells.     In  the  posterior  part  are  centres  for  movements 


-      .^- 


'"•""^'^^WHit 


Fig.  191. — Same.     Superior  surface. 

of  the  head  and  eyes,  and  in  the  left  third  frontal  is  a  centre  for  speech  or  articulation 
memories.  Injuries  of  the  prefrontal  generally  lead  to  changes  of  character,  indi- 
cated by  peevishness  and  irritability  of  temper,  mental  enfeeblement,  lack  of  power 
to  concentrate  the  mind  or  to  control  the  acts  or  emotions.  The  left  lobe  is  said  to 
be  more  important  psychically. 

The  Central  Convolutions. — This  part  of  the  brain  is  called  the  sensori-motor  area, 
because  it  is  concerned  in  the  receipt  and  emission  of  nervous  impiilses  which  lead  to 
voluntary  motions  of  the  body.  Certain  parts  of  this  area  are  in  relation  with  certain 
groups  of  voluntary  muscles  on  the  opposite  side  of  the  body.  These  areas  preside 
not  so  much  over  single  muscles  as  over  those  groups  of  muscles  which  act  together 
in  producing  definite,  purposeful  acts.     The  motor  area  proper  is  confined  to  a  narrow 


ANATOMY  AND  PHYSIOLOGY  OF  THE  BRAIN 


359 


space  on  the  posterior  surface  of  the  precentral  convolution  extending  down  to  the 
bottom  of  the  fissure  of  Rolando.  It  is  co-extensive  with  deposits  of  the  giant  cells 
of  Betz.  (Sherrington  and  Greenbaum).  The  lower  part  of  the  central  convolutions, 
known  as  the  central  operculum,  is  a  centre  for  movements  of  the  larynx,  mouth, 
tongue  and  face.  This  area  reaches  to  the  lower  bend  or  genu  of  the  fissure  of  Rolando, 
near  which  is  the  centre  for  the  neck.  Above  and  occupjang  the  middle  third  of 
the  convolution  are  centres  for  the  shoulder,  arm,  hand  and  fingers,  which  extend  up 
as  far  as  the  upper  genu,  near  which  is  the  centre  for  the  trunk.  Above  this  genu  are 
centres  for  the  hip,  leg,  toes,  the  area  extending  over  into  the  paracentral  lobules.  Near 
the  base  of  the  first  and  second  frontal  convolutions  is  a  centre  for  movements  of 
the  head  and  eyes.  The  exact  arrangement  of  these  centres,  which  has  been  deter- 
mined by  experiments  upon  monkeys  and  other  lower  animals  as  well  as  by  clinical 
and  surgical  observations  on  man,  is  shown  in  the  accompanying  Figs.  190,  191,  192. 
The  posterior  central  convolution  is  probably  the  centre  for  cutaneous  sensations. 


.    ,  fRCCENTRAL 
^-:rU  ,POSTCENTPAL 


'v.^Tl       '^'^n 


si 


Fig.  192. — ^Localization  of  the  functions  of  the  brain.     Lateral  surface. 


The  various  sensori-motor  centres  are  not  sharply  limited,  but  lap  one  over  the 
other,  so  that  the  motor  area  for  the  arm,  for  example,  extends  over  somewhat 
into  that  for  the  shoulder.  The  corresponding  sensory  areas  are  more  diffuse,  so  that 
it  takes  a  much  more  extensive  destruction  of  a  certain  area  of  the  cortex  to  produce 
an  anaesthesia  of  the  arm  than  it  does  to  produce  a  paralysis  of  the  arm.  The  strictly 
motor  and  sensory  areas  have  closely  adjacent  to  them  psychic-motor  and  psychic- 
sensory  areas,  concerned  in  the  higher  elaboration  of  movements,  sensations  and 
reflexes. 

Bilateral  Representation. — Those  muscles  of  the  two  sides  of  the  body  which  act 
together  have  a  double  representation  in  the  brain.  For  example,  each  group  of  mus- 
cles used  in  inspiration  has  a  centre  in  both  hemispheres;  consequently,  when^one 


360 


DISEASES    OF    THE    NERVOUS    SYSTEM 


centre  is  destroyed  no  paralysis  results,  for  the  reason  that  the  other  centre  continues 
its  work.  In  the  same  way  some  of  the  muscles  of  the  face,  such  as  those  for  closing 
the  eyes,  have  a  double  representation,  and  a  lesion  destroying  the  centre  for  the  or- 
bicularis palpebrarum  on  one  side  will  not  usually  cause  paralysis,  because  of  the  con- 
tinued action  of  the  centre  of  the  other  side.  The  more  perfect  and  habitual  the  as- 
sociated action  of  the  muscles  of  the  two  sides  of  the  body,  the  more  completely  can 
one  centre  do  the  work  of  its  associate.  The  best  examples  of  the  muscles  having 
the  double  representation  are  the  orbicularis  palpebrarum,  the  muscles  of  the  vocal 
cords,  the  muscles  concerned  in  deglutition  and  in  respiration.  The  muscles  of  the 
viscera  and  blood-vessels  have  no  known  representation  in  the  cortex  of  the  human 
brain. 

The  special  sensations  have  a  bilateral  representation  also;  but  the  more  specialized 
the  sense  the  less  can  one  hemisphere  take  the  place  of  the  other. 


Fig. 


193. — ^Localization  of  the  functions  of  the  brain  cortex,  showing  the  psychic 
areas.     (Campbell.)     Lateral  surface. 


Parietal  Lobes. — -The  upper  portion  of  the  parietal  lobe  is  the  centre  or  region, 
for  we  include  both  the  cortex  and  its  underlying  tracts,  for  association  of  memories 
of  form,  or  more  properly  the  perception  of  the  form.  When  destroyed  there  is  as- 
tereognosis  or  loss  of  perception  of  form;  and  if  with  it  there  is  some  involvement  of 
the  zone  of  language,  there  is  asymboly;  that  is,  an  inability  to  tell  what  the  object 
is  even  if  the  form  is  recognized.  Lying  anteriorly  in  the  lower  part  of  the  parietal 
convolution  below  the  parietal  fissure,  is  an  area  for  memories  of  muscular  movements, 
and  when  this  is  injured  there  is  ataxia,  or  loss  of  sense  of  position.  The  whole  parietal 
lobe  seems  to  have  to  do  with  association  processes  connected  with  the  elaboration 
of  sensations.  It  is  a  percipient  or,  as  Mills  calls  it,  a  concrete  memory  centre,  not  a 
sensory  centre.  Even  the  ataxia  which  occurs  here  is  a  loss  of  perception,  and  not  a 
pure  sensory  loss. 

In  its  posterior  and  inferior  part,  on  the  left  side,  we  have  part  of  the  zone  of 
language,  particularly  that  concerned  in  memories  of  written  words  (reading  centre). 
Near  this  is,  perhaps,  a  centre  for  memories  of  the  uses  of  things  (praxic  centre). 


ANATOMY  AND  PHYSIOLOGY  OF  THE  BRAIN 


361 


Occipital  and  Temporal  Lobes— Centres  of  Special  Sense. — The  special  senses  have 
two  centres — the  primary  and  the  secondary.  The  primary  centres  are  connected 
with  the  gangUa  at  the  base  of  the  brain;  the  secondary  centres  are  situated  in  the 
cortex. 

The  primary  centre  for  vision  is  in  the  posterior  part  of  the  optic  thalamus,  the 
external  geniculate  bodies,  and  anterior  corpora  quadrigemina.  The  secondary 
centre  is  situated  in  the  occipital  lobe,  and  particularly  upon  its  mesial  surface  and 


VISUO-SENSORY 

Fig.  194.— Localization  of  the  functions  of  the  cortex  of  the  brain,  showing   the 
psychic  areas.     {Campbell.)     Superior  surface. 

about  that  part  of  the  cuneus  known  as  the  calcarine  fissure.  Each  occipital  lobe  is 
the  centre  for  visual  impulses  from  the  corresponding  half  of  the  retina  of  each  eye; 
for  example,  the  left  occipital  lobe  is  the  centre  for  vision  of  the  left  half  of  the  retina 
of  each  eye.  This  relation  is  shown  in  the  diagram  (see  Optic  Nerve).  Total  destruc- 
tion of  both  occipital  lobes,  or  even  of  a  considerable  part  of  them  if  the  destruction 
involves  the  median  surface,  will  cause  bUndness.  Destruction  of  one  lobe  causes 
only  half-blindness  or  hemianopsia. 


362 


DISEASES    OF   THE    NERVOUS    SYSTEM 


The  primary  centre  for  hearing  is  in  the  posterior  tubercles  of  the  corpora  quandri- 
gemina  and  the  internal  geniculate  bodies.  The  secondary  centre  is  in  the  cortex  of 
the  first,  including  the  transverse  convolution  of  the  temporal  lobe.  Destruction  of 
one  temporal  lobe  causes  some  deafness  in  the  opposite  ear.  This  deafness,  however, 
is  not  complete  because  the  sense  of  hearing  has  a  bilatei'al  representation;  each  ear 
in  other  words,  sends  fibres  to  the  temporal  lobes  of  each  side,  although  more  fibres 
cross  over  than  go  to  the  lobe  of  the  corresponding  side.  The  consequence  is  that  the 
loss  of  one  temporal  lobe  is  in  a  measure  supplied  by  the  other  (see  also  Aphasia). 

The  primary  centre  for  smell  is  in  the  olfactory  lobes.  The  secondary  centre  is 
probably  in  the  anterior  part  of  the  limbic  lobe,  the  uncus  and  in  part  of  the  hippo- 
campal  convolution.  Whether  the  tracts  for  the  sense  of  smell  are  connected  with 
the  optic  thalamus  or  other  ganglia  is  not  definitely  known. 

The  primary  centre  for  taste  is  not  known,  but  sensations  of  taste  may  connect 


^POSTCENTRAL  PSYCHIC-SENSORY 
JSrcr/VFRAL  SENSORY 


Fig.  195. — -Same.     Median  surface. 


with  the  optic  thalamus  before  passing  into  the  secondary  centre,  which  is  in  the  hippo- 
campal  convolution. 

Centres  for  Special  Associations. — There  are  certain  sensations,  perceptions  and 
movements,  simple  in  character  and  frequently  repeated,  so  that  they  finally  get  to 
be  used  almost  automatically  in  their  work.  These  impressions  relate  to  the  use  of 
the  muscles  in  speech,  in  writing  and  in  gesture  language;  also  to  other  frequently 
repeated  purposeful  movements  of  the  limbs.  The  muscular  movements  in  writing 
and  speaking  are  so  often  repeated  that  certain  areas  in  the  cortex  are  set  apart  for 
the  memories  of  these  processes,  memory  being  simply  a  revival  and  re-association  of 
previously  registered  impressions.  The  visual  sensations  and  the  ideas  elaborated 
from  them,  which  are  frequently  repeated  in  learning  to  read,  have  also  a  centre  which 
is  set  apart  for  them.  This  forms  a  centre  for  the  memories  of  written  language.  In 
the  same  way  there  are  auditory  sensations  and  ideas  elaborated  and  so  frequently 
repeated  as  to  be  used  automatically  in  acquiring  language.     These  are  stored  up  as 


ANATOMY    AND    PHYSIOLOGY    OF   THE   BRAIN  363 

auditory  memories.  We  have  what  may  be  called  motor  memories  connected  with 
speech  and  gesture.  These  special  memories  have  been  found  to  have  a  certain 
localization  in  the  brain.  The  centre  for  the  memories  of  the  articular  movements 
of  speech  is  in  the  posterior  part  of  the  third  left  frontal  convolution;  the  centre  for 
the  memories  of  the  movements  of  writing  is  not  perfectly  known,  but  is  thought  to 
be  at  the  posterior  part  of  the  second  left  frontal  convolution.  The  centre  for  the 
memories  of  gesture  language  is  unknown.  The  centre  for  the  memories  of  ordinarj^ 
co-ordinate  movements  is  probably  in  the  inferior  parietal  lobule.  The  centre  for 
the  visual  memories  of  written  language  is  in  the  angular  gyrus,  extending  backward 
from  there  into  the  occipital  lobe.  The  centre  for  the  audtiory  memories  of  spoken 
language  is  in  the  posterior  part  of  the  first  and  the  corresponding  upper  part  of  the 
second  temporal  convolution.  In  right-handed  people  the  language  memory  centres 
are  in  the  left  cerebral  hemisphere;  in  left-handed  people  they  are  in  the  right  hemi- 
sphere. The  centres  for  the  memories  and  associations  connected  with  language 
together  form  a  large  area,  known  as  the  zone  of  language.  The  destruction  of  these 
memorj^  centres  produces  different  forms  of  aphasia,  as  will  be  described  later. 

In  addition  to,  disturbances  in  centres  are  produced  by  remote  lesions  which  cut 
off  the  associating  fibres  connecting  these  centres  with  each  other  or  with  motor  or 
sensory  centres  proper,  causing  a  phenomenon  called  diaschesis. 

The  Centrum  Ovale,  Corpus  Callosum,  and  the  Associative  Functions  of  the 
Brain. — The  different  parts  and  centres  of  the  brain  are  connected  together  by  the 
associating  tracts  and  with  lower  levels  by  the  projection  fibres.  The  simpler  and 
less  developed  centres  of  the  two  halves  of  the  brain  are  closely  connected  by  fibres 
that  nm  chiefly  in  the  corpus  callosum.  The  more  highly  specialized  and  less  simple 
in  function  a  centre,  the  less  close  is  its  commissural  connection  and  the  more  inde- 
pendent is  one  half  of  the  brain  from  the  other.  Thus  the  centres  for  the  movements 
of  the  thorax  in  respiration  are  closely  bound  with  each  other;  those  for  the  purposefiil 
movements  of  the  hands  less  so;  those  for  receiving  visual  impressions  are  almost 
independent;  and  the  centres  for  language  associations  which  are  still  more  highly 
specialized,  are  practically  entirely  independent.  We  infer  that  the  higher  mental 
functions,  therefore,  work  either  in  one  cerebral  hemisphere  or  in  the  other,  and  that 
the  two  halves  of  the  brain  do  not  co-operate  with  each  other  in  much  of  the  higher 
intellectual  work.  This,  however,  may  not  be  true  for  the  very  highest  mental  proc- 
esses, though  persons  have  lived  and  shown  fair  intelligence  without  a  callosum. 

The  corpus  callosum  is  the  great  commissural  tract  connecting  the  two  cerebral 
hemispheres  and  their  respective  centres.  The  anterior  commissure  does  some  of 
the  same  work,  being  more  specially  connected  with  the  function  of  olfaction.  The 
posterior  commissure  has  comparatively  few  bilateral  connecting  fibres,  its  function 
being  more  to  connect  the  thalamus  with  the  cranial  nerve  nuclei  and  other  centres 
below. 

The  Corpus  Striatum. — This  ganglion  is  in  relation  with  the  cerebral  cortex  slightly, 
with  the  internal  capsule  slightly,  with  the  thalamus  and  subthalamic  nuclei,  and 
probably  through  these  with  the  cerebellum  and  with  nuclei  in  the  pons.  It  is  also 
in  connection  with  fibres  that  come  up  from  the  muscle-sense  tract,  in  the  spinal  cord. 
It  seems  most  intimately  connected  with  the  thalamus  and  subthalamic  ganglia.  Its 
functions  are  therefore  probably  connected  with  supplementing  automatic  movements. 
Destruction,  of  this  ganglion  in  the  human  brain  produces  at  times  motor  and  vaso- 
motor disturbances.  Lesions  of  it  seem  to  have  to  do  indirectly  with  the  production 
of  tremor  and  rigidity. 

The  Thalamus  Opticus. — The  thalamus  is  in  relation  by  its  projection  fibres  with 
the  frontal,  parietal,  occipital,  and  temporal  cortex.  It  is  in  relation  below  with 
tracts  for  cutaneous  and  deep  sensibility.     The  fibres  that  go  to  the  occipital  cortex 


364  DISEASES    OF    THE    NERVOUS    SYSTEM 

are  connected  with  the  optic  tract,  and  have  to  do  with  the  function  of  vision.  The 
fibres  that  go  to  the  temporal  lobe  are  connected  with  the  auditory  tract,  and  have 
to  do  with  the  function  of  hearing.  The  optic  thalami  have  a  probable  relation 
to  the  expression  of  emotions.  Lesions  of  the  posterior  part  of  the  thalamus  will 
produce  hemianopsia  and  central  pain.  Other  than  this,  lesions  of  the  optic  thalamus 
produce  no  definite  symptoms  which  enable  us  to  make  a  local  diagnosis,  except 
through  injury  of  neighboring  parts.  Disturbances  of  hearing  have  not  certainly 
been  traced  to  lesions  in  the  thalamus.  Lesions  of  the  thalamus  sometimes  produce 
various  forms  of  mobile  spasm,  but  these  are  generally  attributed  to  irritation  of  the 
fibres  of  the  internal  capsule,  which  go  close  to  it.  Hence,  aside  from  pain,  disturb- 
ances of  vision  and  of  deep  sensibility,  the  optic  thalamus  also  must  be  considered 
clinically  a  latent  region. 

The  Corpora  Quadrigemina. — The  anterior  tubercles  of  the  corpora  quadrigemina, 
together  with  the  external  geniculate  bodies,  form  part  of  the  primary  centres  of  vision, 
The  anterior  tubercles,  however,  have  to  do  chiefly  with  reflex  movements  of  the 
pupil  and  the  ciliary  muscles.  The  posterior  tubercles  of  the  corpora  quadrigemina 
and  the  internal  geniculate  body  are  connected  with  the  auditory  nei've,  and  have  to 
do  with  reflex  movements  associated  with  hearing  and  space  sensations.  They  also 
appear  to  receive  some  fibres  from  the  cerebellum;  their  injury  or  disease  produces 
some  disturbances  in  equilibrium  and  possibly  in  hearing.  Owing  to  the  fact  that  the 
nuclei  of  the  third  nerves  and  the  red  nuclei  lie  beneath  the  corpora  quadrigemina, 
lesions  of  these  latter  produce  nystagmus  and  paralyses  of  the  third  nerve,  disturbances 
in  equilibrium,  and  forced  movements.  Lesions  in  this  neighborhood  sometimes  cause 
somnolent  and  stuporous  states. 

The  red  nuclei  are  connected  with  the  anterior  cerebellar  peduncles  on  the  one  hand 
and  with  the  lenticular  nucleus  and  optic  thalamus  and  spinal  cord  on  the  other, 
and  are  concerned  in  securing  muscular  tone,  synergy  and  co-ordination. 

The  Cerebellum. — It  receives  impulses  from  the  cerebral  hemispheres,  and 
these  impulses  go  via  the  pons  to  the  cortex  of  the  lateral  lobes.  It  also  receives 
impulses  from  the  vestibular  and  to  some  extent  from  the  other  sensory  cranial 
nerves.     These  impulses  go  to  the  cortex  of  the  vermis. 

The  cerebellum  also  receives  impulses  from  the  spinal  cord  via  the  direct  (dorsal) 
cerebellar  tract  and  the  column  of  Gowers  (ventral  cerebellar  tract),  but  not  from 
the  posterior  columns.  These  impulses  go  to  the  cortex  of  the  vermis.  The  efferent 
tracts  of  the  cerebellum  are  those  to  the  cerebrum  and  those  to  the  mid-brain,  sub- 
thalamic region  and  spinal  cord.  The  cerebello-cerebral  fibres  leave  the  cortex  of 
the  lateral  lobe,  go  to  the  dentate  nuclei,  thence  through  the  anterior  cerebellar 
peduncles,  crossing,  in  most  part,  to  the  red  nucleus  and  thalamus,  perhaps  to 
the  nucleus  tecti,  thence  to  the  cortex  of  the  brain.  The  cerebello-spinal  fibres 
start  from  the  cortex  of  the  vermis,  then  to  the  roof  and  emboliform  nuclei  (intrinsic 
cerebellar  nuclei),  thence  to  the  nucleus  of  Deiters  mainly  (paracerebellar  nuclei  of 
Horsley),  thence  to  the  spinal  cord  in  the  anterolateral  tracts,  and  anterior  cornua. 
Some  cerebello-spinal  fibres  go  from  the  red  nucleus  and  tectal  nucleus  to  the  cord. 
Hence  we  have  vestibular-spinal,  the  rubro-spinal  and  the  tecto-spinal  tracts  convey- 
ing impulses  down  to  the  cord,  originating  mainly  at  least  in  the  cerebellum.  Horsley 
has  shown  that  the  cerebellar  cortex  always  sends  out  its  efferent  impulses  first 
to  the  various  nuclei  of  the  cerebellum.  Stimulation  of  these  causes  tonic  move- 
ments of  the  head.  Stimulation  of  the  paracerebellar  nuclei  (Deiter's,)  in  the  pons 
also  causes  tonic  movements  of  the  body.  It  is  when  these  intrinsic  and  paracerebellar 
nuclei  are  irritated  that  we  get  cerebellar  fits.  L.  Hill  and  others  have  shown,  as 
Jackson  first  averred,  that  the  cerebellum  causes  tonic  fits,  the  cerebral  hemispheres 
clonic  fits.     There  is  a  nervous  circuit  between  the  cerebrum,  brain  axis,  cerebellum. 


ANATOMY    AND    PHYSIOLOGY    OF    THE   BRAIN  365 

and  spinal  cord.  The  cerebellum  has  thus  the  function  of  organizing  the  higher  auto- 
matic and  psycho-reflex  movements,  and  through  its  relations  with  the  eighth  nei-ve 
and  spino-cerebellar  tiacts  of  enabling  us  to  keep  our  equilibrium  and  maintain  our 
relations  in  space.  It  also  gives  tonus  and  synergy  to  the  muscles.  The  vermis  or 
median  lobe  is  the  part  which  in  man  is  most  important  in  doing  this  work.  The 
lateral  lobes  are  concerned  in  acquiring  new  movements  and  dexterities  and  in  syner- 
gizing  different  segments  of  the  body  (neck,  arms,  legs).     (See  also  Figs.  218.  p.  462.) 

The  pons  Varolii  contains  some  of  the  cranial  nerve  nuclei  and  collections  of  nerve- 
cells  which  are  connected  with  fibres  from  the  cerebral  cortex  on  the  one  hand  and  the 
cerebellum  on  the  other.  It  also  contains  the  long  tracts  of  nerve-fibres  that  pass 
from  the  cerebrum  down  through  into  the  medulla  and  spinal  cord  and  transverse 
tracts  of  fibres  which  connect  the  two  hemispheres  of  the  cerebellum.  Lesions  in  it 
cause  disturbances  in  function  of  the  cranial  nerves  and  of  the  motor,  sensory  and 
commissural  tracts. 

The  medulla  oblongata  contains  centres  of  the  cranial  nerves,  and  in  it  also  are 
various  reflex  and  automatic  centres  controlling  and  regulating  the  vasomotor  system 
respiratory  and  cardiac  rhythm,  visceral  movements  and  secretion. 

The  olivary  bodies  are  connected  with  the  cerebellum,  basal  ganglia,  and  with 
the  spinal  cord.  When  injured,  disturbances  of  equihbrium  and  co-ordination 
occur. 

The  Latent  Regions  of  the  Brain. — There  are  certain  parts  of  the  cerebral  cortex 
destruction  and  irritation  of  which  produce  no  special  and  distinctive  phenomena 
in  man.  These  are  the  greater  part  of  the  temporal  lobe  of  the  right  side  and 
a  portion  of  the  temporal  lobe  on  the  left  side.  A  part  of  the  inferior  parietal  lobule 
also  may  be  regarded  as  a  latent  region.  The  frontal  lobe  we  have  already  spoken  of 
as  being  concerned  with  certain  mental  functions,  but  lesions  here  often  produce  no 
symptoms,  and  may  be  to  a  certain  extent  regarded  as  latent. 

Brain  Size  and  Weight.— The  length  of  the  brain  averages  160  to  170  mm.  and  its 
transverse  diameter  is  140  mm. 

The  female  brain  is  usually  shorter  than  the  male. 

The  average  weight  of  the  male  brain  is  1,358  grams;  that  of  the  adult  female, 
1,245  grams. 

The  weight  varies  with  age,  sex,  race,  and  intelligence,  and  with  a  number  of 
other  factors.  The  average  weight  of  the  brain  at  birth  is  327.8  gm.;  the  brain  grows 
rapidly  until  the  age  of  four,  then  more  slowly  until  the  age  of  seven,  then  very  slowly 
up  to  the  age  of  sixteen  to  twenty.  At  about  the  age  of  forty-five  in  man  and  fifty 
in  woman  it  begins  to  lose  weight  slowly,  and  at  the  age  of  eighty  or  over  it  has  lost 
about  120  gm.  (4  oz.).  The  brain  of  man  weighs  absolutely  about  9  per  cent,  more 
than  that  of  woman.  Relative  to  the  body  weight,  the  brain  weight  of  man  is  about 
2  per  cent.;  that  of  woman  is  very  little  less.  The  sexual  difference  is  extremely 
small.  Brown  finds  that,  after  making  all  allowances,  woman's  brain  weighs  about 
one  ounce  less  than  man's. 

The  brain  weighs  more  in  the  civilized  races,  and  more  in  certain  of  the  civilized 
races  than  others;  the  brains  of  English,  German,  and  Scotch  weigh  more  than  those 
of  French,  Italian,  and  Russian.  Some  of  the  African  and  Australian  tribes  have  the 
smallest  brain,  the  average  negro  brain  weighing  1,250  gm. 

Caucasian  race  average  brain  weight  is  1,335  grams. 
Chinese  race  average  brain  weight  is  1,332  grams. 
Malay  race  average  brain  weight  is  1.266  grams. 
Negro  race  average  brain  weight  is  1,244  grams. 
Australian  race  average  brain  weight  is  1,185  grams. 


366  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  brain  weight  of  highly  civilized  nations  is  somewhat  larger  than  that  of  the 
uncivilized,  and  cultural  activity  in  a  race  rather  slightly  increases  the  cranial  capac- 
ity. When  a  brain  weighs  less  than  1,130  gm.  in  man  or  990  gm.  in  woman,  it  is 
called  a  microcephalic  brain;  if  the  weight  is  above  1,490  gm.  in  man  or  1,345  gm. 
in  woman,  it  is  called  a  megalocephalic  brain. 

Brain  weight  has  a  certain  relation  to  inteUigence,  which  is  not,  however,  an  abso- 
lute one.  Among  a  hundred  men  of  more  than  average  intelligence,  the  percentage 
of  large  brains  would  be  about  25,  whereas  the  percentage  of  large  brains  among  per- 
sons of  ordinary  or  low  intelligence  would  not  be  more  than  4  or  5.  In  estimating 
the  importance  of  brain  weight,  one  must  consider  the  height,  the  weight  or  volume  of 
body,  muscular  mass,  and  superficial  area;  these  are  called  the  somatic  factors.  The 
following  formula  has  been  devised  by  Snell  for  estimating  the  mental  power  of 
different  animals. 

^      Ks 

In  this  formula  P  represents  the  psychical  factor  or  the  amount  of  intelligence, 
H  the  brain  weight,  K  the  body  weight,  S  for  the  somatic  factor.  The  somatic  factor 
has  been  estimated  to  be  for  mammals  about  0.666.  Applying  this  formula,  we  find 
that,  expressed  relatively  the  intelUgence  of  man  equals  0.87;  woman,  0.86;  the  ape, 
0.42;  the  rabbit,  0.59;  the  birds  from  0.167  to  0.09. 

The  brain  weight  as  compared  with  the  body  weight  is  not  so  great  in  man  as  it  is 
in  certain  birds. 

The  weight  of  the  brain  in  the  adult  male  as  compared  with  the  spinal  cord  is 
greater,  however,  than  in  any  other  race.  That  is  to  say,  the  spinal  cord  in  the  human 
subject  weighs  approximately  2  per  cent,  of  the  brain.  In  the  anthropoid  apes  it 
weighs  6  per  cent. ;  in  American  mammals,  from  23  to  47  per  cent. 

The  relative  weight  of  different  parts  of  the  brain  is  about  as  follows:  frontal 
lobes,  28  per  cent. ;  parietal  lobes,  36  per  cent. ;  occipital,  10  per  cent. ;  temporal,  13 
per  cent.;  island  of  Reil,  9  per  cent.;  pons,  1)4  per  cent.  The  cerebellum  weighs 
about  one-eighth  as  much  as  the  cerebrum.  The  proportion  of  the  gray  to  the  white 
matter  in  adults  is  60  to  40  (Vierordt). 


CHAPTER  XVII 

DISEASES  OF  THE  BRAIN  AND  ITS  MEMBRANES 

GENERAL  SYMPTOMS 

General  symptoms  are  developed  when  the  brain  and  its  membranes 
are  subjected  to  irritating  influences.  These  influences  may  be  of  various 
kinds,  and  are  best  illustrated  by  the  irritant  which  occurs  in  the  early 
stages  of  a  febrile  infection  like  meningitis.  Similarly,  general  symptoms 
may  be  caused  by  conditions  which  benumb  and  depress  or  paralyze  the 
activities  of  the  brain.  These  influences  are  either  mechanical,  such  as 
those  of  brain  pressure,  or  perhaps  severely  toxic  such  as  occurs  in  the 
advanced  stages  of  an  inflammation.  Perversions  of  brain  activity  in 
various  directions  partly  irritant,  partly  paralyzing  also  may  occur. 

There  are  also  disturbances  of  brain  function  due  to  irritative  or 
destructive  foci  in  the  brain. 

The  general  symptoms  of  brain  irritation  are  headache,  vertigo,  vomit- 
ing photophobia,  mental  irritabihty,  insomnia,  pecuhar  feelings  of  full- 
ness and  pressure  about  the  head,  noises  in  the  ears  or  in  the  head, 
tenderness  about  the  scalp,  and  in  severe  cases  rigidity  of  the  neck,  con- 
vulsive symptoms  and  delirium. 

The  symptoms  of  depression  of  the  brain  functions  are  often  caused 
by  an  inflammatory  exudate  or  serous  effusion  which  compresses  the 
brain  and  hence  they  are  spoken  of  as  symptoms  of  brain  compression. 
These,  as  they  progressively  increase,  are  headache,  mental  dulness, 
restlessness,  mental  confusion,  clouding  of  consciousness,  delirium,  dis- 
turbed sleep  and  finally  stupor  and  coma.  As  these  symptoms  progress 
there  occur  a  slowing  of  the  pulse,  increased  blood-pressure,  irregular 
respiration,  and  papillary  cedema  of  the  optic  discs.  Finally  the  coma 
deepens,  the  respiratory  and  bulbar  centres  become  paralyzed;  there  is 
now  a  rapid  pulse  and  lowered  blood-pressure,  paralysis  of  respiration  and 
death. 

The  focal  symptoms  of  brain  disease  depend  upon  the  location  of  the 
particular  lesion.  If  it  is  in  the  motor  area  there  will  be  symptoms  of 
spasmodic  character  or  of  a  local  paralysis.  If  it  is  in  the  speech  area 
there  will  be  symptoms  of  aphasia. 

Besides  the  symptoms  which  are  due  to  the  local  disease  there  may 
be  general  symptoms  produced  by  the  pathological  condition.     Thus, 

367 


368  DISEASES    OF   THE    NERVOUS    SYSTEM 

while  a  tumor  of  the  brain  will  cause  perhaps  only  focal  symptoms  of 
irritation  or  pressure,  a  suppuration  in  the  brain  will  produce  general 
symptoms  such  as  are  associated  with  sepsis,  viz.,  chills,  irregular  fever, 
mental  hebetude,  prostration,  emaciation,  and  sweats. 

The  dominant  focal  symptoms  are:  local  convulsions,  hemiplegia, 
hemiataxia,  hemianopsia,  cerebellar  ataxia  and  dyssynergy,  cranial  nerve 
palsies,  and  aphasia. 

Among  these  symptoms  there  is  one  which  deserves  some  preliminary 
general  study,  because  it  is  caused  by  lesions  of  different  kinds  and  occurs 
in  different  forms  of  diseases.  This  symptom  which  we  wish  particularly 
to  study  here  is  aphasia. 

Aphasia. — Aphasia  is  a  disorder  of  the  faculty  of  language ;  and  it  has 
a  number  of  varieties,  in  accordance  with  the  particular  part  of  the  brain 
involved  and  the  particular  portion  of  the  mechanism  of  this  faculty  that 
is  injured.  By  the  faculty  of  language  we  include  the  processes  by 
which  we  hear,  see,  and  appreciate  the  meaning  of  symbols  of  language; 
and  express  to  others  by  voice,  writing,  or  gesture  the  content  of  our 
minds.     Language  has,  therefore,  a  receptive  side  and  an  emissive  side. 

We  may  have  lesions  in  the  brain  which  destroy  that  part  of  the  lan- 
guage faculty  concerned  in  our  power  of  seeing  and  understanding 
written  words  or  the  gesture  language.  In  reading  understandingly 
one  sees  certain  words;  these  words  revive  certain  visual  memories  con- 
nected with  past  perceptions.  Thus  one  sees  the  word  "book;"  this 
suggests  to  him  past  memories  of  form,  color,  tactile  and  other  sensations 
associated  with  the  past  perceptions  of  books.  There  is  a  certain  centre 
in  the  brain  where  these  visual  memories  for  letters  and  words  are  asso- 
ciated. When  this  centre  is  destroyed  the  memories  are  destroyed  and 
the  word  ''book"  or  any  other  written  word  conveys  no  meaning.  The 
patient  can  spell  out  the  letters,  he  can  see  the  letters,  but  he  cannot  read 
any  more  than  if  he  had  never  been  taught.  The  condition  is  known  as 
alexia  or  ivord  blindness. 

Again  a  person  may  have  learned  to  associate  certain  gestures  with 
definite  ideas,  as  the  motion  of  carrying  a  glass  to  the  mouth  suggests 
that  of  drinking,  or  the  motions  of  using  a  knife  and  fork  that  of  eating, 
or  the  motions  of  the  deaf-and-dumb  alphabet  with  certain  words  and 
ideas.  These  memories  of  gesture  language  are  located  in  certain  regions, 
and  when  they  are  destroyed  the  patient  is  no  longer  able  to  understand 
gestures  or  the  sign  language.     This  condition  is  known  as  sign  blindness. 

When  a  person  is  not  able  to  understand  the  significance  or  uses  of 
things  about  him,  he  is  said  to  have  apraxia.  For  example  he  sees  a 
knife  and  names  it  but  he  does  not  know  its  use.  He  knows  its  use  but 
he  does  not  know  how  to  make  the  movements  necessary  to  put  it  to  use. 
In  the  former  case  he  has  sensory  apraxia  (imperception,  agnosia  are 


DISEASES    OF    THE   BRAIN    AND    ITS    MEMBRANES  369 

other  terms).  In  the  latter  case  he  has  motor  apraxia  (also  a  form  of 
agnosia) . 

A  person  hears  certain  words,  as,  for  example,  the  word  "knife." 
This  conveys  to  him  a  certain  idea  of  the  form,  color,  and  other  properties 
associated  with  knife.  The  memories  associated  with  the  auditory  per- 
ception of  different  words  are  stored  up  in  a  certain  locality  which  is  the 
centre  for  auditory  memories.  When  this  centre  is  destroyed  the  person 
hears  spoken  words,  but  they  convey  to  him  no  meaning.  All  that  is 
said  to  him  sounds  as  if  it  were  in  a  foreign  language:  he  hears,  but  he 
does  not  understand.  This  condition  is  known  as  word  deafness,  or  audi- 
tory aphasia.  Varieties  of  auditory  aphasia  occur.  In  some  cases  for 
example,  a  patient  cannot  name  objects  seen,  felt,  heard  or  touched 
(anomia) . 

In  communicating  our  ideas,  we  speak,  write,  and  make  gestures. 
In  speaking  we  make  use  of  the  organs  of  articulation,  and  this  use  in- 
volves the  fine  adjustment  of  a  delicate  muscular  apparatus.  In  the 
act  of  expressing  ideas  we  have  to  bring  into  play  the  memories  of  the 
past  muscular  movements  of  this  articulatory  mechanism.  These  move- 
ments were  learned  by  a  slow  and  painful  process  during  infancy.  After 
the  power  of  speech  is  acquired,  the  mechanism  works  readily  and  almost 
automatically,  because  we  only  have  to  send  a  stimulus  to  the  centre 
which  presides  over  the  stored-up  memories  of  the  impulses  to  innervate 
properly  the  mechanism  of  speech.  There  is,  therefore,  a  centre  for  the 
memories  of  the  movements  of  articulation — a  centre  which  is,  of  course, 
closely  connected  with  the  motor  areas  that  directly  innervate  the  larynx, 
pharynx,  and  oral  and  facial  muscles.  When  a  lesion  destroys  this  centre 
for  speech  memories,  a  person  is  unable  to  reproduce  the  words  necessary 
for  expressing  an  idea;  for  example,  he  sees  a  knife,  he  knows  what  it  is, 
but  the  memory  of  the  motions  necessary  to  express  the  word  "knife" 
is  gone.  To  him  it  seems  that  the  name  is  gone,  and  that  is  the  common 
way  of  expressing  it.  He  cannot  say  the  word  "knife."  The  patient 
may  wish  to  express  the  idea  of  pain.  He  feels  the  pain,  he  knows  that 
he  has  pain,  but  he  cannot  revive  those  motor  memories  which  are  con- 
cerned in  expressing  the  word  "pain;"  he  cannot  tell,  therefore,  in  words 
what  is  the  matter  with  him.  When  a  person  is  thus  troubled,  he  is 
said  to  have  a  form  of  motor  aphasia  for  which  the  particular  name 
given  is  aphemia. 

In  the  same  way  there  is  a  centre  for  the  memories  of  the  muscular 
movements  concerned  in  writing;  and  when  a  lesion  destroys  this  centre 
the  patient  is  unable  to  write,  though  he  may  be  able  to  speak.  This 
condition  is  called  agraphia. 

There  is  a  centre,  less  well  defined,  for  the  memories  of  the  move- 
ments used  in  gesture  language,  and  when  this  is  destroyed  the  person 

24 


370  DISEASES    OF    THE    NERVOUS    SYSTEM 

is  unable  to  express  his  ideas  by  gesture  or  sign  language.  This  condition 
is  known  as  amimia.  A  loss  of  memory  of  musical  expression  is  called 
amusia. 

In  some  cases,  patients  are  able  to  speak  and  write,  but  they  skip 
words,  repeat  often,  and  talk  confusedly.  There  is  here  a  lesion  of  the 
tracts  associating  the  language  centres,  and  the  condition  is  called  con- 
duction aphasia,  while  to  his  stumbling  speech  the  term  paraphasia  is 
given. 

Thus  symptomatically  and  psychologically  we  have  the  following 
forms  of  aphasia: 


Sensory. 


Motor. 


Alexia. 

Sign  blindness. 
Apraxia. 
Word  deafness. 
Aphemia. 
Agraphia. 
Amimia. 
Amusia. 

Conduction  aphasia. 
Mixed  Forms.  \  Paraphasia. 

[  Jargon  aphasia. 

In  the  examination  of  a  case  of  aphasia,  questions  to  bring  out  the 
following  points  should  be  put  to  the  patient: 
To  test  his  power  of  expression: 

1.  Can  he  speak  voluntarily  or  use  ejaculations  expressive  of  some 
emotional  state? 

2.  Can  he  answer  questions? 

3.  Can  he  count  or  repeat  letters  of  the  alphabet? 

4.  Can  he  repeat  words?     If  he  can  talk,  does  he  talk  coherently, 
or  is  it  a  jargon,  or  does  he  skip  words  now  and  then  as  he  talks? 

5.  Can  he  hum  tunes? 

6.  Can  he  write  voluntarily  or  to  dictation?     Can  he  copy? 

7.  Can  he  indicate  his  wants  by  gestures? 
To  test  his  power  of  understanding  language : 

8.  Does  he  understand  the  words  spoken  to  him,  or  gestures  made 
to  him? 

9.  Can  he  name  things  seen,  heard,  felt  or  can  he  name  abstract 
things,  like  darkness,  beauty,  sorrow? 

10.  Can  he  recall  to  his  mind  objects  named  to  him?     That  is,  if 
the  word  "poison"  is  spoken,  does  he  know  what  it  means? 

11.  Can  he  read  silently  or  aloud? 

12.  Does  he  know  the  uses  of  things  about  him,  such  as  how  to  use 
a  knife  and  fork,  or  a  pencil,  and  what  is  his  general  intelligence? 

By  a  series  of  questions  of  this  sort  we  can  make  a  diagnosis  of  the 


DISEASES    OF    THE   BRAIN    AND    ITS    MEMBRANES  371 

psychological  ciuality  of  his  speech  defect,  and  say  that  he  has  "auditory" 
aphasia,  or  "motor"  aphasia,  or  a  "visual"  aphasia,  and  so  on. 

The  physician,  however,  can  ignore  this  kind  of  diagnosis,  to  a  large 
extent,  and  he  had  best  try  first  to  determine  the  anatomical  location  of 
the  aphasia,  and  arteries  involved  in  the  lesion.  By  the  method  of  ques- 
tioning which  has  just  been  laid  down,  the  patient  is  discovered  to  have 
certain  peculiar  defects  of  language,  and,  in  accordance  with  these  de- 
fects, the  physician  is  able  to  assign  the  trouble  to  one  or  another  portion 
of  the  brain. 

1.  Thus,  in  one  very  common  form  of  speech  disturbance,  we  have  a 
fronto-capsular  lesion,  i.e.,  a  lesion  injuring  the  left  third  frontal  convolu- 
tion and  often  extending  back  so  as  to  involve  the  internal  capsule 
somewhat.  Here,  the  patient  has  usually  hemiplegia  but  no  sensory 
disturbance,  and  his  intelligence  is  quite  good.  The  main  characteristic 
of  his  speech  defect  is  that  of  aphemia,  that  is,  a  complete  inability  to 
say  a  word,  or,  at  least,  only  one  or  two  simple  words.  With  this  mutism, 
there  is  also  usually  a  loss  of  ejaculatory  speech,  and  of  responsive  speech, 
of  counting  or  association  speech,  and  of  ability  to  repeat  words  that  are 
spoken.  Yet,  though  thus  completely  aphemic,  the  patient  can  write 
and  read  well,  and  understand  spoken  language  perfectly.  The  lesion  here 
is  in  the  third  left  frontal  convolution,  extending,  perhaps,  somewhat 
into  the  lenticular  zone  (Fig.  173),  and  due  to  involvement  of  one  of  the 
ganglionic  arteries,  which  does  not  supply  much  of  the  corpus  striatum. 
Sometimes  there  is  an  involvement  of  the  cortical  arteries.  Pure  frontal 
lesions  are  very  rare,  because  the  third  frontal  convolution  is  not  sup- 
plied altogether  by  a  single  artery  but  by  several.  Occasionally  this 
portion  of  the  brain  is  rather  extensively  involved,  and  there  may  be  with 
some  hemiplegia,  also  evidences  of  difficulty  in  understanding  spoken 
language.  Sometimes  the  pure  fronto-cortical  lesion  causes  an  aphemia, 
like  this  described,  which  is  temporary,  because  the  lesion  is  so  small. 
This  last  form  of  aphasia  is  sometimes  known  as  "pure  motor"  aphasia 
or  "pure  motor  subcortical"  aphasia. 

2.  The  second  type  of  aphasia  is  an  "occipital "  or  " parieto-occipital " 
aphasia,  known  clinically  as  "pure  alexia." 

In  this  group  of  cases,  the  patient  can  talk  well,  and  understand,  and 
write  well,  but  he  cannot  read,  except  a  few  words  or  letters,  and  he  can- 
not copy  well.  He  has  generally  a  hemianopsia,  and  sometimes  the 
alexia  is  wrongly  attributed  to  this.  Usually  there  is  with  it  some 
hemiataxia  or  hemianesthesia  or  hemiparsesthesia,  and  there  may  be  a 
very  slight  temporary  hemiplegia.  The  intelligence  of  the  patient  is  good. 
These  cases  are  quite  rare  also.  They  are  due  to  a  lesion  in  the  occipital 
lobe,  extending  sometimes  into  the  angular  gyrus.  This  part  of  the 
brain  is  supphed  by  the  posterior  cerebral  artery.     When  lesions  of  this 


372 


DISEASES    OF    THE    NERVOUS    SYSTEM 


artery  occur,  they  involve  the  visual  centre  often,  and  also  the  so-called 
association  or  visuo-psychic  centres  concerned  in  reading.  These  are 
situated  in  the  angular  and  in  the  second  occipital  gyri.  While  the  lesion 
is 'usually  due  to  involvement  of  the  posterior  cerebral,  alexia  may  be 
caused  also  by  lesions  of  the  Sylvian  artery,  since  it  supplies  some  of  the 
angular  gyrus,  but  in  this  case  we  get  some  injury  of  the  temporal  cortex, 
and  an  alexia  which  is  complicated  with  other  symptoms  (Fig.  196.) 

3.  A  third  group  of  aphasias  is  a  "temporal  or  ''parieto-temporal" 
or  the  ''sensory  aphasia  of  Wernicke."  Here  the  patient  is  found  to 
have  no  hemiplegia,  or  only  a  temporary  and  slight  one,  but  his  power 
of  coherent  speech  is  seriously  injured.     He  has  some  voluntary  speech, 


Fig.  196. — ^Lesion  of  Sylvian  artery,  and  softening  of  temporo-parietal  region,  with 

aphasia .     (Spiller.) 


and  responsive  speech,  and  may  use  words  very  fairly,  even  loqua- 
ciously, but  he  talks  nonsense  on  account  of  the  confusion,  repetition 
and  misplacement  of  words.  He  has,  in  other  words,  paraphasia  or 
jargon.  He  cannot  name  objects  shown  him,  and  usually  not  objects 
that  are  heard  by  him,  or  felt,  or  smelt,  or  tasted.  This  constitutes  a 
symptom  known  as  "anomia,"  or  "optic  aphasia."  He  can  read  a  little, 
but  very  poorly,  and  write  a  httle  and  copy,  but  this  is  all  done  very 
badly.  In  other  words,  he  has  some  alexia  and  agraphia.  He  cannot 
understand  questions  or  simple  directions,  or,  if  he  does  understand 
simple  directions,  he  cannot  understand  comphcated  ones,  and  there  is, 
apparently,  some  loss  of  general  intelligence.  Patients  act  sometimes 
rather  childishly  and  emotionally.     Perhaps  the  dominant  symptoms  may 


DISEASES    OF   THE   BRAIN   AND    ITS   MEMBRANES 


373 


be  said  to  be  this  inability  to  understand,  and  together  with  confusion  and 
jargon  or  paraphasia  of  speech.  With  this  speech  defect  there  may  be,  as 
already  stated,  a  temporary  or  slight  hemiplegia.  There  is  usually  some 
hemiansesthesia  or  ataxia  or  astereognosis,  or  all  three  of  them.  There  is 
sometimes  a  hemianopsia,  which  may  not  be  permanent.  Such  persons  im- 
prove a  good  deal  in  their  intelligence,  but  rarely  get  entirely  normal,  and 
they  have  to  be  watched  rather  carefully.  They  do  not  show  symptoms 
of  any  true  dementia.  The  lesion,  in  these  cases,  is  in  the  auditory  and 
the  auditory  psychic  area  of  Campbell,  that  is  to  say,  in  the  posterior 
two-fifths  of  the  first  temporal  convolution,  extending,  in  severe  cases, 
into  the  parietal  lobe  or  into  the  second  temporal.  There  is  a  cutting 
off,  to  some  extent,  of  the  association  tracts  between  the  auditory  psy- 


FiG.  197. — Showing  the  zone  of  language  and  the  localization  of  the  four  types  of 
aphasia.  I.  Frontocapsular  aphasia,  characterized  by  aphemia.  II.  Parietooccipi- 
tal aphasia,  characterized  by  alexia.  III.  Temporal  or  temperoparietal  aphasia, 
characterized  by  anomia,  some  mind  deafness,  and  paraphasia.  A  small  lesion  may 
cause  only  optic  aphasia.  IV.  Frontolenticular  aphasia,  the  common  type  of  aphasia, 
characterized  by  aphemia  with  much  agraphia,  alexia,  mind  deafness,,and  hemiplegia. 


chic  and  the  visual  area.  The  artery  here  involved  is,  of  course,  one  of 
the  terminal  branches  of  the  Sylvian,  or  perhaps  the  trunk  of  the  Sylvian 
itself.  In  this  latter  case,  when  the  lesion  is  extensive,  the  speech  is  apt 
to  be  very  confused,  and  almost  purely  jargon,  and  there  is  more  likely 
to  be  some  hemiplegia.  Occasionally,  a  very  small  lesion  of  the  first 
temporal  alone  occurs,  and  here  the  patient  is  simply  unable  to  name  ob- 
jects seen,  and  often  objects  that  are  felt,  or  heard,  or  smelt,  or  tasted. 
In  this  case,  we  have  what  is  called  a  "pure  anomia,"  or  inability  to  name 
things.     Another  term  for  is  is  ''optic  aphasia." 

4.  The  fourth  group  of  aphasias  is  the  "fronto-lenticular"  or  "len- 
ticular zone"  aphasia  and  "mixed"  aphasia.  This  is  the  most  common 
of  all  aphasias.     We  here  find  a  very  extensive  aphemia,  that  is,  inability 


374  DISEASES    OF    THE    NERVOUS    SYSTEM 

to  talk  voluntarily  or  even  to  say  any  words.  There  is  a  considerable 
loss  of  ability  to  read  and  reading  is  always  imperfect;  that  is,  there  is 
some  alexia;  there  is  also  some  difficulty  in  understanding,  at  least  compli- 
cated sentences;  that  is,  there  is  some  mind  deafness.  There  is  always  a 
very  decided  hemiplegia,  but  rarely  any  sensory  symptom.  The 
lesion  here  involves  the  branch  of  the  middle  cerebral  that  supplies  the 
corpus  striatum,  the  internal  capsule,  and  the  fibres  converging  into  it 
from  the  second  and  third  frontal  and  precentral  convolution.  In  other 
words,  the  lenticular  zone  is  involved  and  part  of  the  fibres  that  come  from 
the  temporal  and  frontal  areas  of  speech  are  destroyed.  In  some  way 
also,  the  association  tracts  from  the  occipital  lobe  must  be  affected,  be- 
cause of  the  difficulty  in  reading. 

This  form  of  aphasia,  which  I  call,  anatomically,  the  "lenticular  zone" 
aphasia,  is  called  by  Marie,  an  anarthria  plus  the  aphasia  of  Wernicke. 
The  accompanying  diagram  will  show  the  anatomical  localization  of  the 
four  different  groups  of  aphasias.  And  I  am  sure  that  the  student  and 
physician,  in  attempting  to  make  a  diagnosis  of  aphasia,  will  find  the 
task  much  lightened  by  turning  his  attention  to  the  effort  to  locate, 
anatomically,  the  area  of  the  brain  and  the  artery  involved. 

Conduction  and  Mixed  Aphasia. — There  are  very  few  cases  of  pure 
conduction  aphasia.  When  it  occurs  there  is  paraphasia  and  paragraphia ; 
the  patient  repeats  words  over  and  over  in  a  kind  of  verbal  intoxication, 
or  mixes  things  so  that  the  speech  is  almost  gibberish.  Still  he  can  ex- 
press himself  and  can  write,  read  and  understand.  The  lesion  is  usually 
in  the  island  of  Reil  or  the  convolutions  about  the  fissure  of  Sylvius.  It  is 
a  lenticular  zone  aphasia. 

Practically,  conduction  aphasia  is  usually  mixed  with  a  visual  or 
auditory  aphasia. 

Thus  we  have  the  following  groups  of  aphasia : 

Clinical  Type  Anatomical  Seat 

1.  Pure  motor  aphasia.  Fronto-cortical  aphasia. 
Pure  agraphia.  Fronto-cortical  aphasia. 

2.  Pure  alexia.  Occipital  or  parieto-occipital  aphasia. 
Apraxia. 

3.  Auditory  aphasia. 

Anomic  aphasia.  Tempo ro-parietal  aphasia. 

(Sensory  aphasia  of  Wernicke). 

4.  Mixed  and  conduction  aphasias.  Lenticular  and  fronto-lenticular  aphasia. 

MALFORMATIONS  OF  THE  BRAIN  AND  ITS  ENVELOPES 

Congenital  malformations  of  the  brain  are  of  little  practical  importance,  for  in 
most  cases  the  monsters  cannot  live  and  in  all  cases  they  are  better  dead.  I  shall 
simply  give  a  brief  enumeration  of  the  important  forms. 


DISEASES    OF    THE   BEAIN    AND    ITS    MEMBRANES  375 

I  Anencephaly. 

Abnormalities  I  Micrencephaly  and  microcephaly. 

of  the  brain.  |  Porencephaly. 

[  Absences  or  malformations  of  parts,  e.g.,  cyclopia. 

Acrania. 

Meningocele. 

1  I  Encephalocele. 

its  envelopes.      __    ,  ,    ,       , 

[  Hydrencephalocele. 


Abnormalities 
of  brain  and 


Anencephaly  is  always  present  with  acrania.  In  anencephaly  the  cerebellum  and 
part  of  the  basal  ganglia  may  be  present.     In  such  case  the  child  can  live  a  short  time. 

Micrencephaly  and  Microcephaly. — Micrencephaly  is  a  condition  in  which  the 
brain  is  only  partially  developed.  If,  as  is  usually  the  case,  the  cranium  is  also  ab- 
normally small,  it  is  called  microcephaly.  It  is  due,  probably,  in  all  cases  to  an  in- 
herent defect  in  the  growth  of  the  brain.  Virchow  has  asserted,  however,  that  there 
is  a  form  in  which  the  abnormality  is  caused  by  a  premature  growing  together  of  the 
cranial  bones,  a  micrencephaly  being  a  result  of  the  mechanical  condition.  An  adult 
cranium  whose  great  circumference  measures  less  than  43  cm.  will  contain  a  micren- 
cephalic  brain.  The  normal  minimum  weight  of  the  adult  brain  is  960  grams  for  man 
and  880  for  woman.  It  should  bear  the  ratio  to  the  body  at  birth  of  14  per  cent., 
and  of  2.37  per  cent,  in  adult  life  (Vierordt). 

Porencephaly  is  often  an  artificial  condition.     It  will  be  described  later. 

In  cyclopia  there  is  an  undivided  anterior  cerebral  vesicle;  the  orbits  form  a  con- 
tinuous cavity  with  a  single  rudimentary  eye. 

Meningocele  is  a  hernia  of  the  brain  membranes,  arachnoid,  and  dura  mater 
through  a  cleft  in  the  skull.  In  encephalocele  the  brain  also  protrudes.  Both  these 
forms  occur  usually  in  the  occipital  region  and  almo«t  invariably  in  the  median  line. 
In  hydrencephalocele  there  is  a  sac  with  fluid  contents. 

DISEASES  OF  THE  MEMBRANES  OF  THE  BRAIN 

The  diseases  to  be  considered  under  this  head  are  anaemia  and  hyper- 
semia,  inflammation  of  the  dura  mater  or  pachymeningitis  and  inflamma- 
tion of  the  pia  mater  or  leptomeningitis. 

Anaemia  and  Hyperaemia  of  the  Membranes  of  the  Brain. — ^Ansemia  of 
the  membranes  of  the  brain  is  a  condition  that  cannot  be  separated  from 
anaemia  of  the  brain  substance,  and  will  be  considered  in  connection  with 
it.  Hyperaemia  of  the  brain  membrane,  so  far  as  it  relates  to  hyperaemia 
of  the  pia  mater,  must  also  be  considered  in  connection  with  hyperaemia 
of  the  brain  tissue.  Dural  hyperaemia,  or  congestion  of  the  dura  mater,  is 
a  condition  which  occurs  as  the  result  of  injuries,  sunstroke,  and  of  cer- 
tain infective  poisons,  especially  that  of  syphilis.  The  symptoms  are 
those  of  pachymeningitis  of  the  slight  grade,  and  will  be  described  under 
that  head.  They  consist  mainly  of  pain,  occasional  attacks  of  vertigo, 
and  sensations  of  fullness  about  the  head.  The  treatment  is  that  for  the 
beginning  stages  of  a  meningitis. 

Inflammation  of  the  Dura  Mater  or  Pachymeningitis  Externa. — It 
has  been  the  custom  to  describe  two  forms  of  pachymeningitis,  the  ex- 


376  DISEASES  or  the  neevous  system 

ternal  and  the  internal.  Internal  pachymeningitis,  or  hsematoma  of  the 
dura  mater,  is  properly  a  hemorrhagic  disorder,  and  is  described  under 
the  head  of  Dural  Hemorrhages.  A  true  inflammation  confined  to  the 
internal  surface  of  the  dura  alone  is  of  extremely  rare  occurrence. 

Pachymeningitis  externa  is  a  disease  that  involves,  at  first  at  least,  the 
outer  surface  of  the  dura,  and  is  usually  of  surgical  origin  and  interest. 

Etiology. — Accidents,  injuries,  osteitis,  caries  of  the  petrous  bone  in 
mastoid  disease,  of  the  ethmoid  bone  in  ozsena,  necrosis,  syphilis  and  ery- 
sipelas are  the  usual  causes. 

The  symptoms  are  local  headache,  fever,  delirium,  sometimes  even 
convulsions  and  paralysis.  In  the  severe  cases  the  disease  has  usually 
extended  and  involved  the  pia.  Pus  is  generally  formed,  and  burrows 
between  the  bone  and  dura.  The  disease  is  recognized  mainly  by  the 
discovery  of  the  local  cause.  The  course  is  acute  or  subacute.  The 
treatment  is  a  surgical  one. 

Inflammations  of  the  Pia  Mater. —  Cerebrospinal  Meningitis. — In- 
flammation of  the  pia  mater  has  the  following  types:  (1)  Acute  puru- 
lent meningitis  due  to  various  forms  of  pyogenic  organisms  other  than  the 
meningococcus;  (2)  epidemic  cerebrospinal  meningitis  due  to  a  specific 
meningococcus  infection;  (3)  tuberculous  meningitis;  (4)  serous  men- 
ingitis and  (5)  syphilitic  meningitis. 

Most  of  all  these  forms  of  meningitis  may  be  either  acute  or  chronic 
the  chronic  form  being  usually  simply  a  sequela  of  the  acute. 

ACUTE  PURULENT  CEREBROSPINAL  MENINGITIS 

Etiology. — Acute  leptomeningitis  is  due  to  an  infective  process. 

The  infecting  organism  is  usually  a  streptococcus,  pneumococcus,  or 
staphylococcus.  The  meningitis  caused  by  the  meningococcus  is  of  a 
special  type  described  later.  The  streptococcus  is  the  most  frequent  in- 
fecting organism.  The  infection  is  almost  always  secondary  to  a  focal 
lesion  or  general  infection. 

The  commonest  focal  lesions  are  disease  of  the  ear,  and  of  the  nose  and 
accessory  sinuses.  Fractures  of  the  skull  and  other  wounds  of  the  head,  or 
spine  may  become  infected  and  lead  to  meningitis.  Over-doses  of  sal- 
varsan  introduced  into  the  spinal  canal  may  cause  by  chemical  irritation  a 
meningitis.     Brain  abscess,  and  infected  sinus  thrombosis  may  be  causes. 

Just  now  it  is  stated  that  purulent  meningitis  is  seen  most  often  by 
obstetricians  from  sepsis  and  by  otologists  and  rhinologists. 

Pneumonia  is  the  most  frequent  infective  disease  in  which  the  pyogenic 
organisms  are  carried  by  the  blood.  After  this  come  erysipelas,  sepsis, 
scarlet  fever,  more  rarely  endocarditis,  empyema,  rheumatism,  measles, 
typhoid  fever  and  mumps.  Alcoholism  and  a  generally  lowered  state  of 
vitality  from  malnutrition  predispose  to  the  infection.     Insolation  can 


DISEASES    OF   THE  BRAIN   AND    ITS   MEMBRANES  377 

of  itself  not  cause  it.  The  disease  is  more  frequent  in  males,  and  is  dis- 
tributed through  all  ages  of  life,  though  it  occurs  oftener  in  the  young. 

Symptoms.^ — ^The  symptoms  in  the  various  types  differ  somewhat,  but 
have  a  general  similarity.  They  are  to  be  broadl}^  grouped  into  the 
prodromal,  the  irritative,  the  depressive,  and  the  paralytic  stages. 

Prodromal  symptoms  are  shorter  and  less  marked  in  simple  meningitis 
than  in  tubercular.  They  are  really  the  symptoms  of  a  general  infection. 
The  patient  suffers  from  malaise,  languor,  headache,  vertigo,  irrita- 
bility, loss  of  appetite  and  vomiting.  Of  these  sj'-mptoms  headache  is  the 
most  notable. 

[The  description  of  the  symptoms  of  epidemic  cerebrospinal  menin- 
gitis given  later  answers  for  the  common  purulent  form,  except  for 
certain  variant  types.] 

Course  and  Duration.^ — The  disease  may  begin  suddenly,  and  the 
patient  pass  at  once  into  the  comatose  state,  dying  in  a  few  days.  Usually 
the  process  lasts  one  or  two  weeks;  it  may  be  prolonged  for  several  weeks. 

The  prognosis  is  very  grave,  but  it  is  less  serious  than  in  tuberculous 
meningitis  and  more  serious  than  in  the  cerebrospinal  form. 

The  diagnosis  is  based  on  the  presence  of  an  exciting  cause,  such  as 
disease  of  the  ear  or  nose,  trauma,  infective  fevers,  and  upon  the  presence 
of  the  symptoms  given.  It  is  usually  easily  recognized,  the  main  difficulty 
being  to  distinguish  it  from  other  forms  of  meningitis. 

To  determine  this,  it  is  advisable  to  make  a  lumbar  puncture,  draw 
off  the  fluid,  and  examine  it  for  bacteria  and  the  presence  of  cellular 
elements.     (See  Epidemic  Cerebrospinal  Meningitis.) 

Pathology. — The  disease  is  a  fibro-purulent  or  purulent  inflammation. 
It  involves  usually  the  base  more  than  the  convexity,  but  the  reverse  may 
happen.  The  ventricles  are  often  involved  and  may  be  independently 
inflamed.  There  are  descriptions,  therefore,  of  simple  basilar  meningitis, 
meningitis  of  the  convexity,  and  ventricular  meningitis  or  ependymitis. 
The  inflammatory  deposits  are  most  conspicuous  along  the  course  of  the 
Sylvian  fissure  and  the  vessels  branching  from  it,  about  the  optic  chiasm, 
and  at  the  posterior  and  under  surface  of  the  cerebellum  and  the  sides  of 
the  pons.  It  may  lie  only  in  the  subarachnoid  cavity,  but  usually  the 
arachnoid  and  sometimes  the  dura  are  implicated.  There  is  increase 
of  fluid  in  the  ventricles  and  arachnoid  cavities,  and  this  fluid  may  be  tur- 
bid.    The  surface  of  the  ventricles  may  show  an  inflammatory  process 

The  micro-organisms  found  in  meningitis  are  as  already  stated  the 
pneumococcus,  the  streptococcus,  the  staphyloccus  and  a  bacillus  re- 
sembling that  of  typhoid  fever.  Still  others  have  been  described,  and 
the  process  may  be  a  mixed  infection. 

Treatment. — Prophylaxis  is  the  most  important  measure,  as  there  is 
no  specific  treatment.     Chronic  disease  of  the  ear  and  nasal  sinuses  should 


378  DISEASES    OF    THE    NERVOUS    SYSTEM 

be  attended  to,  and  injuries  of  the  skull  treated  with  the  strictest  regard 
to  antisepsis.  When  the  disease  is  developed,  the  indications  are  to  treat 
the  original  focus  of  infection  (ear,  etc.)  to  open  the  skull  and  decompress 
and  drain  in  certain  cases ;  to  combat  the  general  sepsis.  The  treatment  is 
therefore  often  a  surgical  one.  To  combat  the  infection  there  are  im- 
munizing sera  from  which  not  much  has  been  accomplished.  Flushing 
the  blood  with  intravenous  injections  of  saline  tranfusions,  epidermo- 
clysis  and  proctoclysis  may  be  tried.  Urotropin  and  formaldehyde  have 
not  proved  useful.  Recently  the  use  of  watery  solutions  of  sulphate  of 
magnesium  have  been  strongly  recommended. 

EPIDEMIC  CEREBROSPINAL  MENINGITIS 

{Spotted  Fever) 

Cerebrospinal  meningitis  occurs  as  an  epidemic  and  endemic  disease 
caused  by  the  diplococcus  intracellularis  meningitis. 

It  is  a  disease  which  has  invaded  practically  all  of  Europe  and  has 
occurred  in  the  East  and  in  Africa.  The  most  extensive  epidemics 
have  occurred  in  the  United  States,  affecting  all  the  states  and  spreading 
to  Canada,  but  not  to  the  countries  in  the  South.  The  disease  occurs 
sporadically  in  the  large  cities  of  the  United  States  during  the  winter. 
The  epidemic  occurs  periodically  at  irregular  times.  The  disease  occurs 
at  all  ages  but  children  are  the  most  affected. 

In  New  York  City  about  two-thirds  of  the  cases  were  in  children  under 
ten  years  of  age,  but  about  16  per  cent,  occurred  in  persons  over  twenty 
and  it  may  attack  persons  as  old  as  fifty.  The  sexes  are  about  equally 
affected.  Race  and  nationality  seem  to  have  no  particular  influence 
although  in  the  South  the  negroes  are  less  affected  than  the  whites. 

The  disease  occurs  in  the  winter  months,  beginning  sometimes  in  late 
October  and  ending  in  May  but  sometimes  not  beginning  until  the  first 
month  of  the  spring.  Unusually  cold  weather  seems  to  be  associated  with 
the  height  of  the  epidemic. 

The  disease  is  most  prevalent  among  poor  and  in  over-crowded  dwell- 
ings.   In  New  York  three-fourths  of  the  patients  lived  in  tenement  houses. 

The  disease  is  very  shghtly  infectious.  Fatigue  and  ill  health  pre- 
dispose somewhat  to  its  development.  The  infection  occurs  through 
the  nose  and  throat,  and  nasopharyngitis  predisposes  to  the  entrance  of 
the  organism.  The  organism  is  carried  by  healthy  individuals  and  the 
disease  is  propagated  to  a  great  extent  through  these  carriers.  It  has 
been  estimated  that  during  an  epidemic  there  are  ten  to  thirty  healthy 
carriers  in  proportion  to  each  single  person  who  actually  has  the  disease. 
The  nasal  and  oral  secretions  of  the  healthy  carriers  give  positive  cultures 
of    meningococci.      Usually    the     organism    spontaneously    disappears 


DISEASES    OF    THE   BRAIN    AND    ITS    MEMBRANES  379 

from  the  nasopharynx  of  the  carrier  in  a  few  clays,  but  there  are  in- 
stances in  which  a  healthy  person  may  harbor  the  coccus  for  one  or  more 
months. 

The  invasion  of  the  body  by  the  meningococcus  is  probably  accom- 
plished by  the  passage  of  the  organisms  from  the  nasopharynx  into  the 
blood  stream,  resulting  in  a  primary  bactersemia,  and  later  the  bacteria 
become  localized  in  the  meninges.  It  is  possible  that  the  meningococcus 
passes  directly  into  the  cranial  cavity  from  the  nose  and  throat  by  means 
of  the  lymphatics,  but  the  weight  of  evidence  is  against  the  view. 

Pathology. — An  exudation  of  serum,  fibrin,  and  pus  covers  the  pia 
of  the  brain  and  cord  and  infiltrates  its  meshes.  There  is  some  involve- 
ment of  the  superficial  layers  of  the  cortex  in  the  inflammatory  process. 
The  blood-vessels  of  the  meninges  are  engorged  and  surrounded  by  a 
cell  infiltration.  The  inflammation  extends  along  the  sheaths  of  the 
cranial  nerves  and  also  into  the  ventricles.  The  ventricles  are  dis- 
tended with  a  mixture  of  cerebrospinal  fluid  and  exudate,  and  their  walls 
are  red  and  oedematous.  The  cerebrospinal  fluid  is  increased  in  quantity. 
In  chronic  cases  the  pia  arachnoid  may  show  some  cicatricial  thickening. 
The  organism,  a  Gram-negative,  biscuit-shaped  diplococcus,  is  to 
be  found  in  the  exudate  and  in  the  cerebrospinal  fluid,  where  it  is  seen 
in  the  polynuclear  leukocytes  and  also  free.  It  may  be  obtained  by 
culture  from  the  nasopharynx  and  from  the  blood. 

Symptoms. — The  disease  begins  as  a  constitutional  infection  produced 
by  the  passage  of  the  organism  into  the  general  system  and  this  is  fol- 
lowed by  local  symptoms  produced  by  the  localization  of  the  organism 
in  the  meninges.  The  period  of  incubation— i.e.,  the  time  between  the 
invasion  and  the  development  of  the  constitutional  symptoms,  probably 
ranges  between  one  and  five  days. 

The  constitutional  symptoms  corresponding  to  the  period  of  simple 
bactersemia  are  very  much  like  those  of  influenza.  The  disease  comes  on 
acutely  with  chilly  feelings  or  a  severe  chill.  There  is  fever,  throbbing 
headache,  restlessness,  irritability,  and  vomiting.  The  mind  is  clear 
but  the  patient  is  over-sensitive.  Often  the  pupils  are  dilated  and  slug- 
gish, and  there  may  be  photophobia.  A  little  early  stiffness  of  the  neck 
and  tenderness  at  the  angle  of  the  jaw  may  be  present.  Herpes  and  a 
petechial  eruption  are  occasionally  seen.  Sometimes  there  is  irregularity 
in  breathing,  particularly  while  the  patient  is  asleep.  Deep  and  un- 
controllable sighing  is  quite  common.  The  temperature  varies;  some- 
times it  is  very  high,  and  sometimes  low.  In  young  children  there  may 
be  a  little  bulging  of  the  fontanelles,  and  in  adults  Macewen's  sign  can 
often  be  obtained.  It  consists  in  a  dull  tympanitic  note  brought  out 
by  percussing  with  the  finger  over  the  fronto-parietal  region  of  the  skull. 
It' is  most  easily  obtained  if  the  patient's  head  is  lifted  a  little  and  bent 


380  DISEASES    OF   THE    NERVOUS   SYSTEM 

slightly  toward  the  side  to  be  examined.  The  sign  indicates  an  excessive 
amount  of  fluid  in  the  ventricles.  Blood  examination  at  this  stage  usually 
shows  a  moderate  leukocytosis  with  relative  polynucleosis.  Lumbar 
puncture  reveals  an  increase  of  pressure.  The  fluid  is  usually  perfectly 
clear,  however,  although  a  few  free  meningococci  are  sometimes  to  be 
found.  These  symptoms  usually  last  for  twenty-four  to  thirty-six  hours, 
when  the  meningeal  symptoms  make  their  appearance.  In  some  cases  the 
pre-meningitic  symptoms  are  entirely  absent,  and  in  others  a  history  of 
them  is  obtained  only  by  careful  questioning  of  the  family. 

The  stage  of  active  meningitis  begins  with  an  increase  of  all  the  fore- 
going symptoms.  The  headache  becomes  terrific  and  the  patient  com- 
plains of  it  bitterly.  A  number  of  general  convulsions  may  occur,  par- 
ticularly in  children.  Sometimes  consciousness  is  suddenly  lost.  There 
is  extreme  restlessness  and  frequently  delirium.  Vomiting  is  frequent 
and  severe,  and  in  many  cases  uncontrollable.  Usually  it  is  independent 
of  nausea,  and  it  may  be  projectile.  The  patient  suffers  severe  pain  in 
the  back  of  the  neck,  along  the  spine,  and  in  the  legs.  The  neck  becomes 
stiff,  the  head  may  be  retracted,  and  in  some  cases  there  is  rigidity  of  the 
spine  or  opisthotonos.  Photophobia  is  often  very  marked.  The  patient 
is  greatly  prostrated.  Active  delirium  and  restlessness  alternate  with 
deep  stupor,  in  which,  however,  the  patient  usually  shows  some  response 
if  he  is  disturbed.  There  may,  however,  be  periods  in  which  the  mind  is 
clear.  The  patient's  face  bears  an  anxious  expression  and  often  is  cy- 
anosed.  The  rigidity  of  the  neck  may  be  so  great  that  with  a  hand 
placed  under  the  patients  head  one  can  lift  his  body  from  the  bed  with- 
out there  being  any  appreciable  bending  of  the  neck.  An  attempt  to 
move  the  neck  in  any  direction  is  very  painful,  and  there  is  tenderness 
to  pressure  on  the  posterior  neck  muscles.  The  pupils  are  generally 
dilated,  and  react  to  light  sluggishly  or  not  at  all.  Often  there  is  some 
strabismus,  which  may  be  transitory.  Other  cranial  nerve  palsies  may 
occur,  and  there  may  be  clonic  or  tonic  spasms  of  the  extremities.  In 
young  children  there  is  pronounced  bulging  of  the  fontanelles.  Tache 
cerebral  is  readily  obtained.  Kernig's  sign  is  early  and  constant  (Figs.  195, 
198).  This  test  is  made  by  flexing  the  patient's  thigh  to  a  right  angle  on 
the  abdomen  and  then  attempting  to  extend  the  leg  on  the  thigh.  This 
attempt,  in  meningitis  cases,  is  resisted  by  a  sudden  spasm  of  the  ham- 
string muscles  and  the  patient  cries  out  in  pain.  The  abdominal  reflexes 
are  often  missing.  The  tendon  jerks  frequently  are  absent,  but  they 
may  be  exaggerated.  Rarely  there  is  a  dorsal  flexor  response  of  the  toe. 
Brudzinski's  signs  of  meningitis  may  be  present.  In  the  first  sign,  if  one 
of  the  patient's  thighs  is  flexed  upon  the  abdomen  as  far  as  possible  (the 
leg  being  flexed  on  the  thigh),  the  patient  then  draws  up  the  other  into  a 
similar  position.     In  the  second,  with  one  leg^and  thigh  extended  and 


DISEASES    OF    THE   BRAIN    AND    ITS    MEMBRANES  381 

the  other  flexed  as  before,  the  flexed  Hmb  is  lowered  to  the  extended 
position  by  the  examiner,  whereupon  the  patient  draws  up  the  other 
limb  to  a  position  of  flexion  on  the  abdomen.  The  ''neck  sign"  of 
De  Lepinay  can  usually  be  obtained.  It  consists  of  a  flexion  of  the  knees 
and  thighs  which  occurs  when  one  attempts  to  bend  the  patient's  neck 
forward. 

Most  cases  of  meningitis  show  some  respiratory  irregularity.  Connor 
and  Stilmann  found  Cheyne-Stokes  breathing  in  53  per  cent,  of  their 
cases  and  Blot's  breathing  in  27  per  cent.  In  only  5  per  cent,  of  all  their 
cases  did  they  fail  to  find  some  sort  of  irregularity  of  breathing.  Blot's 
breathing  ("cerebral  breathing")  is  thought  to  be  typical  of  meningitis 
as  distinguished  from  other  cerebral  conditions  causing  disturbances 
of  breathing.  It  is  characterized  by  periods  of  apnoea  of  varjdng  length 
and  occurring  at  irregular  intervals  (as  distinguished  from  the  rhythmical 


Fig.  198. — The  Kernig  sign. 

periods  of  apncea  in  Cheyne-Stokes  breathing  which  alternate  with  periods 
of  gradually  increasing  and  gradually  decreasing  respiratory  movement), 
constant  irregularity  in  the  rhythm  and  the  force  of  individual  respira- 
tions, and  the  frequent  occurrence  of  deep  sighing  respirations. 

The  temperature  in  meningitis  is  usually  very  irregular.  It  may  be 
extremely  high  (106°  F.),  or  it  may  be  little  above  normal.  A  septic  tem- 
perature may  occur,  or  the  fever  may  be  high  continuously.  The  pulse 
rate  is  also  irregular.  It  may  be  very  slow — 50  or  less — -but  more  often 
it  is  rapid.  The  pulse  may  be  intermittent  or  show  frequent  changes 
in  rate. 

Generalized  skin  eruptions  occur  in  only  a  small  percentage  of  cases. 
Petechise  if  present  are  usually  profuse,  and  are  distributed  all  over  the 
trunk  and  extremities.  Purpuric  eruptions  do  occur,  but  are  less 
common.     Herpes,  however,  is  a  skin  condition  very  commonly  found. 


382  DISEASES    OF   THE    NERVOUS    SYSTEM 

Lumbar  puncture  shows  that  the  intra-spinal  pressure  is  abnormally 
increased.  The  fluid  is  turbid,  globulin  and  albumin  tests  are  strongly 
positive,  and  cells  are  numerous,  most  of  them  being  polynuclears — • 
100  per  cent,  in  some  cases.  Stained  smears  from  the  sediment  obtained 
by  centrifuging  show  the  meningococcus^ — in  varying  numbers — i.e., 
Gram-negative,  biscuit-shaped  cliplococci,  both  intra-  and  extra-cellular. 
Cultures  show  a  growth  of  the  meningococcus  after  eighteen  to  twenty- 
four  hours'  incubation.  Elser  and  Huntoon  were  able  to  make  a  posi- 
tive diagnosis  from  the  examination  of  the  spinal  fluid  in  92.5  per  cent, 
of  over  200  cases  examined.  No  altogether  satisfactory  serological 
tests  for  meningitis  have  yet  been  devised. 

Blood  examination  shows  a  leukocytosis  of  between  20,000  and  45,000. 
The  polynuclears  are  markedly  increased,  there  is  a  relative  decrease 
in  the  large  mononuclears,  and  in  very  young  children  a  lymphocytosis 
had  been  observed  in  rare  instances.  The  meningococcus  can  be  obtained 
from  the  blood  by  culture  in  a  certain  number  of  cases.  Elser  had  positive 
results  in  26.5  per  cent,  of  the  cases  examined. 

Course  and  Prognosis.- — The  disease  may  run  a  short  and  malignant 
course  killing  the  person  in  a  few  hours  or  one  or  two  days.  In  moderate 
cases  it  lasts  two  or  three  weeks.  A  large  number  of  different  varieties 
of  the  disease  have  been  described,  such  as  the  abortive  form,  the  ful- 
minating form,  and  the  typhoid  form.  Affections  of  the  joints  are  the 
most  frequent  complications  of  the  disease.  There  may  also  occur  septic 
pneumonia,  pyelitis,  ulcerative  endocarditis,  pericarditis,  neuritis,  and 
phlebitis.  In  some  cases  the  disease  leaves  a  chronic  hydrocephalus, 
and  there  may  be  some  permanent  mental  impairment.  Permanent 
paralysis  of  some  of  the  cranial  nerves,  or,  much  more  rarely,  of  one  or 
more  of  the  extremities  may  occur.  Deafness  is  quite  common,  and 
blindness  and  other  eye  troubles  sometimes  are  observed. 

A  certain  type  of  case  lapses  into  a  state  of  chronic  meningitis, 
which  runs  a  course  of  a  few  weeks'  to  two  or  three  months'  duration,  and 
usually  terminates  fatally.  It  is  characterized  by  extreme  emaciation 
and  severe  cerebral  pressure  symptoms.  The  temperature  is  extremely 
irregular.  It  may  be  normal  or  subnormal,  or,  after  having  been  low  for 
a  considerable  time,  suddenly  rises  and  remain  high  and  irregular.  Chills 
may  occur  irregularly.  The  emaciation  is  most  remarkable.  Though 
many  of  these  patients  take  large  quantities  of  food  and  appear  to  digest 
it  properly,  they  become  rapidly  reduced  to  skeletons,  the  like  of  which 
is  hardly  to  be  seen  in  any  other  disease.  The  patient  is  usually  drowsy 
and  stupid  but  there  may  be  active  delirium.  Complete  coma  occurs 
in  the  final  stages.  The  patient's  eyes  are  wide  open  and  the  face  ex- 
pressionless. Spasms  and  convulsions  are  common.  Vomiting  is  fre- 
quent and  the  bowels  are  constipated.     Macewen's  sign  or  bulging  of 


DISEASES    OF    THE   BRAIN    AND    ITS    MEMBRANES  383 

the  fontanelles  may  be  present.  Rigidity  of  the  neck  and  Kernig's  sign 
usually  continue  present,  but  not  always  so.  The  respirations  are  slow 
and  irregular,  and  the  pulse  rapid,  weak,  and  intermittent.  Strabismus 
or  some  cranial  nerve  paralysis  is  usually  present.  The  tendon  jerks 
are  absent  or  diminished.  Incontinence  of  urine  and  faeces  is  practically 
invariable.     Bed-sores  develop  readily. 

Another  form  of  chronic  meningitis,  the  so-called  posterior  basic 
meningitis  is  distinguished  by  the  fact  that  there  occurs  a  shutting  off 
of  the  communication  between  the  ventricles  and  the  sub-arachnoid 
space.  The  inflammatory  process  thus  becomes  encapsulated  in  the 
ventricles,  and  whatever  inflammation  was  going  on  in  the  subarachnoid 
space  usually  subsides  so  that  the  fluid  obtained  by  lumbar  puncture 
may  be  sterile.     More  commonly,  no  fluid  at  all  is  to  be  obtained. 


Fig.  199. — Cerebrospinal  meningitis,  terminal  stage. 

The  condition  of  posterior  basic  meningitis  may  develop  at  the  outset 
of  the  infection,  but  more  commonly  it  appears  in  the  course  of  a  sub- 
acute or  ordinary  chronic  meningitis. 

The  symptoms  are  those  of  a  rather  mild  sepsis  with  marked  cerebral 
pressure.  The  rigidity  of  the  neck  and  retraction  of  the  head  are  ex- 
treme, and  a  high  degree  of  opisthotonos  is  the  rule.  The  patient  is  apa- 
thetic and  stuporous,  and  convulsions  are  very  common.  Usually  the 
patient  lies  motionless  with  the  extremities  rigid  in  tonic  spasm.  The 
"hydrocephalic  cry"  which  is  altered  at  intervals  without  relation  to 
pain  or  other  stimulation  is  a  common  symptom.  The  eyes  are  wide 
open,  the  lids  retracted,  the  pupils  do  not  react  to  light,  and  there  may 
be  some  exophthalmos.  Various  palsies  are  present.  The  patient  may 
remain  in  this  condition  for  several  weeks.  There  is  practically  always 
a  fatal  termination. 

The  prognosis  of  the  usual  form  of  meningitis  is  always  grave.     The 


384  DISEASES    OF   THE    NERVOUS   SYSTEM 

mortality  in  different  epidemics  has  varied  from  20  to  80  per  cent. 
Only  a  small  percentage  of  those  cases  that  become  chronic  recover. 
Sophian  thinks  that  the  development  of  Biot's  breathing  in  either  acute 
or  chronic  cases  is  of  prognostic  value  indicating  almost  without 
exception  a  fatal  termination. 

Diagnosis.— The  differential  diagnosis  of  epidemic  cerebrospinal 
meningitis  is  to  be  made  from  tuberculous  meningitis,  from  meningitis 
caused  by  strepto-  and  staphylococci,  the  pneumococcus,  and  other 
pyogenic  organisms;  from  poliomyelitis  with  meningeal  symptoms,  and 
from  the  so-called  meningismus  which  occurs  in  various  infectious  diseases. 

Meningitis  due  to  streptococci,  pneumococci,  and  similar  organisms 
presents  the  same  clinical  picture  that  is  found  in  epidemic  meningitis. 
The  history  of  an  epidemic,  on  the  one  hand,  or  of  some  preceding  focus 
of  infection,  as  for  instance  otitis  media  or  broncho-pneumonia  on  the 
other,  may  help  toward  making  a  diagnosis.  Ordinarily,  a  positive  differ- 
ential diagnosis  can  be  made  only  through  the  results  of  the  examination 
of  the  cerebrospinal  fluid. 

In  tuberculous  meningitis  as  a  rule  the  children  are  younger — two 
years  or  less  of  age.  A  family  history  of  tuberculosis  may  be  obtained, 
or  some  family  form  of  tuberculosis  can  be  made  out.  The  child  is 
apathetic  and  stuporous  instead  of  irritable  and  restless.  Cranial  nerve 
palsies  occur  early.  Rigidity  of  the  neck  and  Kernig's  sign  are  usually 
moderate  and  the  temperature  at  first  is  not  very  high — 101  to  102. 
There  is  no  eruption.  The  course  is  acute  and  death  occurs  in  two  to 
four  weeks  after  the  beginning  of  the  disease.  Lumbar  puncture  gives 
an  abundant  fluid,  which  usually  is  clear  with  white  specks  of  fibrin 
floating  in  it.  If  the  fluid  is  allowed  to  stand  for  a  time  a  network  of 
fibrin  forms.  There  is  a  lymphocytosis  instead  of  a  polynucleosis.  Care- 
ful search  may  reveal  the  presence  of  the  tubercle  bacilli,  and  cultures 
fail  to  show  the  diplococcus  intracellularis  or  other  pyogenic  organisms. 
In  the  cerebral  type  of  poliomyelitis  the  patient  is  apathetic  and 
stuporous,  but  he  can  be  roused  and  when  this  is  done  his  mind  is  quite 
clear  and  he  can  answer  questions  intelligently.  Though  there  is  rest- 
lessness and  irritability  these  symptoms  are  much  less  marked  than  in 
meningitis.  Rigidity  of  the  neck  and  Kernig's  sign,  if  present,  are  not 
very  marked.  The  profound  disturbances  of  respiration  and  pulse  which 
occur  in  meningitis  are  absent  in  poliomyelitis.  The  paralyses  in  polio- 
myelitis occur  early  and  are  comparatively  extensive,  while  in  meningitis 
the  palsies  occur  later  and  ordinarily  are  less  extensive.  Usually  in 
poliomyelitis  the  constitutional  and  the  cerebral  symptoms  rapidly  im- 
prove as  soon  as  the  paralyses  occur,  while  in  meningitis  the  occurrence 
of  the  palsies  is  ordinarily  attended  by  an  exacerbation  of  the  constitu- 
tional and  cerebral  symptoms.     The  fact  that  poliomyelitis  is  a  summer 


DISEASES    or    THE   BRAIN    AND    ITS    MEMBRANES  385 

disease  and  meningitis  a  winter  one  should  not  be  forgotten  in  making 
a  diagnosis. 

The  fluid  obtained  by  lumbar  puncture  in  poliomyelitis  is  clear  with 
white  flecks  floating  in  it,  and,  in  fact,  appears  altogether  like  that  ob- 
tained in  tuberculous  meningitis.  There  is,  however,  less  tendency  for 
it  to  form  a  fibrin  network  on  standing,  and,  if  a  network  does  form,  it  is 
less  dense  than  in  the  tubercular  condition.  The  fluid  is  usually  less 
abundant  and  under  less  pressure.  Globulin  tests  are  positive,  but  less 
strongly  so  than  in  meningitis.  The  cells  are  increased  but  not  to  the  ex- 
tent to  be  found  in  meningitis  and  there  is  usually  a  lymphocytosis.  In 
short  the  fluid  findings  of  poliomyelitis  are  much  more  likely  to  be  con- 
fused with  those  of  tuberculous  meningitis  than  of  the  epidemic  variety. 
Bacteriological  examinations  of  the  fluid  are  negative  for  tubercle  bacilli 
and  other  organisms,  and  the  inoculation  of  guinea-pigs  as  a  test  for 
tuberculosis  is  negative. 

The  diagnosis  of  meningitis  from  meningismus  is  usually  not  diffi- 
cult. The  presence  of  the  primary  disorder  causing  the  meningismus  can 
usually  be  made  out.  Unless  there  is  delirium  the  patient  is  clear  and 
intelligent  and,  though  irritable,  does  not  show  the  same  crying  and  com- 
plaining that  occurs  in  meningitis.  Kernig's  sign,  bulging  of  the  fon- 
tanelles,  and  Macewen's  sign  are  moderate  or  absent.  Lumbar  puncture 
settles  the  question  if  the  diagnosis  cannot  be  made  without  it. 

Treatment. — Prophylaxis. — Cases  of  epidemic  meningitis  should  be 
quarantined  until  cultures  from  the  nasal  and  pharyngeal  secretions  are 
negative  for  the  meningococcus.  Healthy  people  who  come  in  contact 
with  these  patients  should  be  examined  in  the  same  way,  and  if  their 
cultures  are  positive  they  should  be  quarantined  also,  and  directed  to  use 
a  disinfecting  spray  of  hydrogen  peroxide,  preceded  by  salt  solution, 
until  negative  cultures  are  obtained,  thus  doing  away  with  the  danger 
of  their  infecting  others  or  of  becoming  infected  themselves. 

The  general  treatynent  is  directed  toward  supporting  the  patient  and 
combating  the  toxaemia.  Sustaining  food  should  be  given  and  such  stimu- 
lants as  digitalis  when  indicated.  Bromides,  chloral  and  morphine  are 
used  as  sedatives.  Ice  bags  to  the  head  and  cool  bathing  for  high  tem- 
peratures are  also  employed.  Lumbar  puncture  is  employed  for  the 
purpose  of  diminishing  pressure  by  draining  off  the  fluid. 

The  specific  treatment  consists  in  the  administration  of  the  Flexner 
serum.  A  lumbar  puncture  is  done  and  the  cerebrospinal  fluid  allowed 
to  flow  until  it  comes  from  the  needle  at  the  rate  of  one  drop  every  three 
to  five  seconds,  which  indicates  roughly  that  about  the  normal  degree 
of  pressure  has  been  attained.  Then  from  5  to  40  cc.  of  the  Flexner 
serum,  depending  on  the  age  of  the  patient,  is  slowly  and  carefully  in- 
jected into  the  spinal  canal  through  the  puncture  needle.     The  safest 

25 


386  DISEASES    OF    THE    NERVOUS    SYSTEM 

method  of  injecting  the  serum  is  that  of  allowing  it  to  flow  into  the  spinal 
canal  by  gravity,  using  instead  of  a  syringe  a  funnel  attached  to  a  twelve 
inch  tube,  and  watching  the  blood  pressure  meanwhile  as  an  index  of 
when  the  flow  should  be  stopped.  A  fall  in  blood  pressure  of  10  mm.  of 
mercury  indicates  that  enough  serum  has  been  injected  (Sophian). 
The  injections  are  repeated  every  day  for  three  or  four  days  and  then 
less  often.  The  best  guide  to  the  proper  frequency  of  the  injections  is  the 
examination  of  stained  smears  from  the  sediment  from  the  fluid.  As 
the  patient  responds  to  treatment  the  number  of  the  cocci  decreases  and 
those  that  are  found  are  intra-cellular.  Numerous  and  extra-cellular 
organisms  indicate  that  an  injection  is  required  on  the  following  day. 
The  use  of  this  serum  has  given  very  satisfactory  results.  In  different 
epidemics  where  a  mortality  of  from  50  to  90  per  cent,  occurred  in  those 
cases  not  treated  with  serum,  the  mortality  was  reduced  to  between  13 
and  50  per  cent,  by  its  use.  H.  W.  Frink,  M.  D. 

TUBERCULOUS  MENINGITIS 

This  is  a  form  of  meningitis  due  to  infection  with  the  bacillus  tuber- 
culosis. It  differs  pathologically  from  other  forms  in  the  character  of 
the  infective  organism ;  anatomically,  in  the  fact  that  the  inflammation  is 
usually  and  chiefly  basilar  and  never  purely  purulent;  etiologically,  in 
that  it  chiefly  affects  young  children;  and  symptomatologically,  in  the 
presence  of  prodromata  and  a  more  irregular  course. 

Etiology. — Tuberculous  meningitis  occurs  chiefly  between  the  ages 
of  two  and  ten,  oftenest  between  two  and  five  years,  sometimes  in  in- 
fancy, rarely  in  adult  life,  very  rarely  after  the  age  of  fifty.  Males  are 
rather  more  subject  to  it.  A  hereditary  history  of  phthisis,  bad  hygienic 
surroundings,  and  the  presence  of  tuberculosis  elsewhere  in  the  body 
predispose  to  it.  Tuberculous  milk  is  probably  one  source  of  the  in- 
fection. The  eruptive  fevers,  especially  measles,  blows  on  the  head, 
and  great  emotional  excitement  appear  to  act  as  exciting  causes. 

Symptoms. — The  child  in  the  prodromal  stage  becomes  peevish,  irri- 
table, loses  interest  in  its  play,  the  appetite  is  gone,  and  there  may  be 
explosive  vomiting.  Sleep  is  restless  and  disturbed.  Paroxysms  of 
severe  headache  occur.  After  two  or  three  weeks,  or  sooner,  these 
symptoms  increase;  the  child  becomes  dull,  moody,  weak,  and  takes  to 
his  bed.  He  lies  there  with  clouded  consciousness,  dozing  at  intervals; 
often  the  cheeks  are  ruddier  than  usual.  Occasionally  he  utters  a  piercing 
cry  as  if  in  great  pain.  He  is  easily  disturbed  by  noises,  and  shows 
himself  generally  hypersesthetic.  He  sighs  deeply,  picks  his  lips  or  the 
bedclothes.  The  neck  is  now  felt  to  be  rather  stiff;  the  reflexes  are  in- 
creased; and  the  abdomen  retracted  or  perhaps  distended.  The  tem- 
perature runs  an  irregular  course  but  is  not  high.     The  pulse  is  slowed 


DISEASES    OF    THE    BRAIN    AND    ITS    MEMBRANES  387 

and  irregular,  sometimes  becoming  very  fast  on  slight  exertion.  The 
respiration  is  disturbed  and  sighing.  The  pupils  are  often  uneven, 
usually  contracted,  and  do  not  react  well  to  light.  The  patient  finally 
passes  into  deep  coma,  with  rise  of  temperature.  The  picture  is  now  one 
of  the  last  stages  of  meningitis,  and  death  occurs  in  about  three  weeks. 
The  special  symptoms  and  signs  of  meningitis  of  other  types  are  present 
in  this  later  stage.  The  condition  of  the  cerebrospinal  fluid  is  described 
elsewhere.     (See  Epidemic  Cerebrospinal  Meningitis). 

Pathological  Anatomy. — In  rapidly  fatal  cases,  with  severe  symptoms, 
there  may  be  only  an  intense  congestion  of  the  brain  with  numerous 
miliary  tubercles  in  the  pia  mater  at  the  base  and  over  the  convexity. 
Here  we  must  assume  that  a  bacillary  toxin  causes  the  symptoms.  In 
most  cases  there  are  decided  deposits  of  tubercles  at  the  base,  with 
fibrinous  inflammatory  deposits  about  the  optic  chiasm,  along  the  fissure 
of  Sylvius,  at  the  sides  of  the  pons,  and  elsewhere.  Miliary  tubercles 
are  seen  scattered  over  the  convexity  and  in  the  choroid  and  ventricles. 
They  are  generally  found  in  the  spinal  membranes  also,  especially  over 
the  Cauda  equina.  The  tubercles  lie  beneath  the  pia  surrounding  the 
small  vessels.  They  may  coalesce  into  large  tuberculous  nodules.  There 
is  usually  an  increase  in  the  arachnoid  fluid,  and  in  most  cases  an  increase 
in  the  ventricular  fluid.  Somewhat  rarely  there  are  very  great  distention 
of  the  ventricles  and  compression  of  the  convolutions.  Small  spots  of 
softening  may  be  seen  from  obliteration  of  the  vessels  by  the  tubercles. 
The  bacillus  tuberculosis  is  found  in  the  tuberculous  nodules. 

Diagnosis. — As  regards  the  form  of  the  disease,  this  is  based  on  the 
hereditary  history,  the  age,  the  existence  of  tuberculosis  of  the  lungs  or 
other  organs,  and  the  peculiar  prodromata  of  the  disease.  Occasionally 
tubercles  can  be  seen  on  the  choroid.  Lumbar  puncture  of  the  spinal 
canal  with  withdrawal  of  fluid  and  its  examination  furnishes  the  most 
certain  method  of  diagnosis.     (See  diagnosis  of  meningitis.) 

Prognosis. — This  is  usually  absolutely  bad,  yet  post-mortem  observa- 
tion of  patients  dying  with  practically  no  inflammatory  change  makes 
it  seem  possible  that  the  disease  might  be  checked,  and  a  good  many 
cases  are  reported  in  which  this  apparently  has  been  done.  Some  of 
these  are,  however,  probably  cases  of  hereditary  syphilis. 

Treatment.- — So  far  as  is  now  known,  this  is  not  different  from  that 
given  under  the  head  of  meningitis  elsewhere. 

HYDROCEPHALUS 

Hydrocephalus  is  a  condition  in  which  there  is  an  excessive  amount 
of  fluid  in  the  ventricles  and  subarachnoid  or  subdural  cavity  of  the 
brain.  When  this  fluid  is  in  the  ventricles  it  is  called  internal  hydro- 
cephalus, and  practically  most  hydrocephalus  is  internal.     In  external 


388 


DISEASES    OF    THE    NERVOUS    SYSTEM 


hydrocephalus  the  fluid  is  in  the  subarachnoid  or  subdural  spaces.  Ex- 
ternal and  internal  hydrocephalus  may  coexist.  Hydrocephalus  is  a 
symptom  of  several  morbid  conditions,  but  in  general  we  may  divide  it 
into  the  chronic  primary  and  secondary  symptomatic  forms. 

Chronic  Primary  Hydrocephalus. — This  is  a  disease  of  infancy,  char- 
acterized by  a  gradual  enlargement  of  the  head,  with  mental  deficiency 
and  symptoms  of  brain  irritation  caused  by  an  accumulation  of  fluid  in 
the  ventricles  of  the  brain. 

Chronic  hydrocephalus  is  not  an  inflammatory  process,  but  one  due 
to  mechanical  causes  or  to  defects  in  structure  or  development.  The  fluid 
always  accumulates  in  the  ventricles  of  the  brain;  hence  chronic  hydro- 
cephalus is  always  internal.  The  so-called  external  forms  of  hydro- 
cephalus are  inflammatory  or  else  are  secondary  to  meningeal  hemorrhage 
or  brain  atrophy. 

Etiology. — Four  out  of  five  cases  begin  at  birth  or  within  the  first 
six  months  of  life.    Congenital  anomaly,  intra-uterine  meningitis,  syphilis, 


'Si^- 

•  •  \ 

•■:"*'"  1-^-W 

^ 

^  ~1^i 

^^^^^^^^^^^^^^^^m^^^m 

Fig.  200. — Chronic  hydrocephalus. 

alcoholism,  lead  poisoning  in  the  parents,  and  some  unknown  family  taint 
predispose  to  the  disease.     Malnutrition  and  rickets  are  also  factors. 

Symptoms. — The  head  may  be  so  large  at  birth  that  instrumental 
help  is  needed.  More  often  the  parents  notice  a  gradual  increase  in  the 
size  of  the  child's  head,  beginning  soon  after  birth.  The  forehead  bulges, 
the  occiput  stands  out,  the  fontanelles  and  sutures  widen,  and  pressure 
shows  evidence  of  fluctuation.  Meanwhile  the  face  does  not  grow  much 
and  the  result  is  to  give  triangular  shape  to  the  head.  It  may  measure 
twenty-four,  twenty-seven  and  one-half  (Minot),  thirty-two  (Bright), 
and  even  forty-three  inches  (Klein)  in  diameter.  These  extreme  measure- 
ments are  reached  only  after  one  or  two  years.  With  this  abnormal 
growth  of  the  head,  mental  and  physical  symptoms  appear.  The  infant 
is  restless  and  irritable;  its  appetite  may  be  good,  but  the  general  nutri- 
tion is  poor  and  its  bodily  growth  is  retarded.  The  mind  does  not  de- 
velop; usually  it  does  not  or  cannot  learn  to  walk.     It  may  be  unable 


DISEASES    OF   THE   BRAIN    AND    ITS    MEMBRANES  389 

to  support  the  weight  of  its  head.  There  is  strabismus  and  sometimes  optic 
atrophy.  The  pressure  of  the  dropsy  thins  the  orbital  bones  and  forces 
down  the  axis  of  the  eyeballs  (see  Fig.  200).  Vomiting,  coma,  and  con- 
vulsions eventually  appear,  and  the  child  usually  dies  of  exhaustion  or 
some  intercurrent  disease  in  two  or  three  years. 

In  some  cases  the  trouble  is  less  serious,  it  ceases  to  progress,  the 
bones  solidify,  and  the  child  grows  up  with  good  intelligence. 

The  hydrocephalus  which  is  associated  with  the  brain  atrophy  of 
insanity  and  old  age  (hydrocephalus  ex  vacuo)  or  with  general  dropsical 
conditions  has  no  kinship  with  the  process  we  are  now  describing. 

Pathology. — The  disease  is  due  to  the  gradual  accumulation  of  a 
serous  fluid  in  the  ventricles  of  the  brain.  The  cause  of  this  is  an  in- 
flammatory or  developmental  obliteration  of  the  aqueduct  of  Sylvius 
or  the  foramen  of  Magendie  and  the  adjacent  lateral  foramina  of  Luschka. 
This  prevents  the  escape  of  the  ventricular  fluid  into  the  subarachnoid 
cavity.  Contributing  factors  are  congenital  or  acquired  defect  in  the 
villous  processes  of  the  pia  arachnoid,  by  which  the  fluid  normally  is  able 
to  pass  into  the  venous  circulation;  and  a  rachitic  and  easily  yielding 
skull.  Hydrocephalus  is  not,  therefore,  an  inflammatory  but  a  mechan- 
ical process.  The  lateral  ventricles  when  the  cerebrospinal  fluid  is  secreted 
are  principally  and  often  solely  affected,  and  these  are  so  distended  as 
to  press  out  their  cerebral  walls,  flattening  the  convolutions  and  turning 
them  into  a  thin  shell  often  less  than  a  quarter  of  an  inch  in  thickness. 
Sometimes  only  one  lateral  ventricle,  and  in  rare  cases  only  the  fourth 
ventricle,  is  affected  by  the  dropsy. 

The  diagnosis  has  to  be  made  from  rickets  and  an  acute  inflammatory 
process.  In  rickets  the  head  is  square,  the  fontanelle  does  not  bulge, 
the  enlargement  is  less,  and  there  are  signs  of  the  disease  in  the  bones 
elsewhere. 

Prognosis. — The  congenital  cases  usually  result  fatally  in  a  few 
months,  or  at  least  before  the  third  year.  Those  developing  in  infancy 
may  persist  for  four  to  six  years;  and  in  mild  cases  the  disease  ceases  to 
progress  and  a  fairly  healthy  adult  life  is  reached. 

Treatment. — A  great  many  measures  have  been  recommended,  but 
there  is  no  unanimity  about  them.  The  inunction  of  mercury  and  the 
administration  of  iodide  of  potassium  combined  with  intravenous  in- 
jections of  salvarsan  are  indicated  if  tests  show  the  presence  of  syphilis. 

Tapping  the  ventricles  in  various  ways  has  been  recommended,  but 
I  have  seen  no  good  results.  Tapping  the  spinal  cord  every  three  days 
and  later  every  week  is  said  to  be  of  some  service. 

Secondary  or  acquired  hydrocephalus  is  usually  caused  by  an  attack 
of  acute  meningitis,  or  by  tumors.  It  may  also  be  due  to  ependymal  in- 
flammation and  to  obstruction  of  the  veins  of  Galen  by  thrombosis  or 


390  DISEASES    OF    THE    NERVOUS    SYSTEM 

other  mechanical  cause.  In  acute  meningitis  this  is  a  frequent  condition 
and  cause  of  death.  In  other  cases  infants  survive  the  meningitis  and, 
with  a  growing  head,  develop  symptoms  later  of  the  hydrocephalus.  In 
the  acute  conditions  the  symptoms  may  run  a  varying  course  owing  to  the 
partial  and  irregular  escape  of  the  fluid.  The  patient,  if  the  disease 
progresses,  becomes  stupid  and  comatose  and  develops  paraplegia  and 
rigidity  of  the  body,  retraction  of  the  head  and  trunk,  and  great  emacia- 
tion. The  treatment  is  the  same  as  that  for  the  primary  form  and  con- 
sists in  puncture  of  the  ventricle  or  corpus  callosum  and  withdrawal  of 
fluid  or  a  decompressive  operation  (Gushing).  The  results  of  surgical 
interference  have  so  far  not  been  satisfactory. 

ALCOHOLIC   "MENINGITIS"    (SEROUS   MENINGITIS,   "WET-BRAIN") 

Alcoholic  meningitis  is  a  clinical  term  used  to  indicate  the  peculiar 
group  of  cerebral  symptoms  which  is  seen  in  persons  who  have  succumbed 
to  the  effects  of  prolonged  alcoholic  intoxication.  The  disease  is  not  a 
true  meningitis  but  an  acute  toxaemia  of  the  brain  with  serous  effusion; 
but  it  may  be  called,  for  the  purpose  of  convenience,  an  alcoholic  serous 
meningitis.  It  should  not  be  confounded  with  the  acute  serous  menin- 
gitis following  infections  and  trauma. 

Etiology. — -The  disease  occurs  oftenest  in  men  simply  because  of  the 
more  frequent  indulgence  of  the  male  sex  in  alcohol.  It  rarely  develops 
until  a  person  has  been  drinking  eight  or  ten  years,  and,  consequently, 
affects  people  oftenest  between  the  ages  of  thirty  and  forty.  The  excit- 
ing cause  is  commonly  alcohol  and  in  this  country  whiskey  or  what  are 
known  as  ''hard  drinks,"  but  beer  and  ale  will  accomplish  the  same  re- 
sult. I  have  rarely  seen  the  disease  in  wine  drinkers.  The  persistent 
use  of  morphine,  cocaine,  and  chloral  may  lead  to  much  the  same  con- 
dition. The  exciting  cause  is  usually  a  continuous  drinking  bout  of 
two  or  three  weeks,  ending  in  delirium  tremens.  The  delirium  tremens, 
however,  is  not  by  any  means  always  present.  The  patient  may  pass 
from  a  condition  of  prolonged  intoxication  into  the  condition  of  alcoholic 
meningitis  or  "wet-brain." 

Symptoms. — In  case  delirium  tremens  has  occurred,  the  patient  after 
two  or  three  days  of  prolonged  delirious  excitement  gradually  sinks  into 
a  semicoma.  This  is  accompaDied  by  a  muttering  delirium.  The 
patient  is  sufficiently  conscious  to  have  flitting  delusions  and  hallucina- 
tions of  sight  and  hearing.  At  this  time  he  is  able  to  drink  and  take 
food;  the  pulse  is  rather  rapid,  the  temperature  is  usually  normal  or  may 
be  raised  one-half  or  one  degree.  The  skin  is  hypersesthetic  and  pressure 
upon  the  muscles  of  the  arms  or  legs  or  abdomen  causes  pain.  The  pupils 
are  usually  rather  small.  Often  at  this  time  conjunctivitis  and  keratitis 
may  appear.     After  a  few  days  the  patient's  stupor  becomes  deeper  and 


DISEASES    OF    THE   BRAJN    AND    ITS    MEMBRANES  391 

he  can  be  aroused  only  with  difficulty.  The  arms  and  legs  are  now 
somewhat  stiff,  the  reflexes  are  exaggerated,  the  neck  is  somewhat  stiff 
and  slightly  retracted,  and  attempts  to  move  it  cause  expressions  of  pain. 
The  Kernig  sign  is  present.  The  abdomen  is  retracted  and  the  skin  and 
muscles  are  still  very  hyper  aesthetic.  The  lids  are  closed.  The  pupils 
are  small  and  do  not  react  well  to  light.  The  tongue  is  coated  and  usually 
dry,  and  urine  and  faeces  may  be  passed  involuntarily.  The  patient  may 
linger  this  way  for  several  days  more.  The  pulse  becomes  rapid  and 
feeble,  the  extremities  are  stiff  and  cold.  The  skin  is  dry  and  loses  its 
elasticity,  so  that  when  pulled  up  between  the  fingers  it  stays  in  folds. 
"Putty  skin  "  is  a  good  name  for  this.  The  coma  deepens,  the  temperature 
may  rise  to  103°  or  104°,  and  symptoms  of  pneumonia  may  appear  as  the 
scene  closes.  On  the  other  hand  in  some  cases  the  patient  does  not  pass 
into  the  worst  stage,  the  mind  becomes  clearer,  the  hypersesthesia  lessens, 
food  is  taken  better,  and  the  bowels  are  moved  voluntarily.  Improve- 
ment continues  and  in  three  or  four  weeks  the  convalescence  begins. 

Pathological  Anatomy. — I  have  made  autopsies  and  careful  micro- 
scopical examinations  in  over  twenty  cases  of  the  character  just  described. 
In  nearly  all  the  brain  is  found  to  be  somewhat  pale,  the  arachnoid  con- 
tains two  or  three  ounces  of  serous  fluid,  the  subarachnoid  space  is  satu- 
rated with  fluid,  and  the  ventricles  are  dilated.  Sections  through  the 
brain  sometimes  show  punctate  hemorrhages  and  in  rare  cases  spots 
of  hemorrhagic  extravasation  are  seen  surrounded  by  softening.  Oc- 
casionally the  beginning  of  a  suppurative  cerebral  meningitis  will  be  seen. 
Microscopic  examination  shows  in  the  uncomplicated  cases  that  there  is 
no  true  inflammatory  process.  There  is  often  congestion,  but  not  always; 
the  commoner  condition  is  an  oedema  of  the  brain  tissue,  the  perivascular 
and  pericellular  spaces  being  dilated.  The  nerve-cells  show  various 
stages  of  degeneration,  not  pigmentary  in  character,  however.  The 
chromophilic  granules  are  often  unstained,  or,  if  stained,  have  lost  their 
true  relations,  and  seem  broken  down.  The  cell  outlines  are  irregu- 
lar; the  nucleus  lies  near  the  periphery  of  the  cell,  and  in  some 
cases  has  broken  out  and  escaped  from  it.  Sometimes  there  is  a  large 
number  of  neuroglia  cells  in  the  pericellular  spaces.  The  disease  is  un- 
doubtedly, primarily  at  least,  a  toxaemia  not  due  directly  to  the  influence 
of  alcohol  but  to  the  poisons  which  have  developed  in  the  body  as  a  result 
of  the  condition  of  inanition  and  the  paralysis  of  the  digestive  function 
caused  by  the  prolonged  ingestion  of  alcohol  and  abstinence  from  food. 
The  cell  degeneration  is  more  like  that  which  is  known  as  "degeneration 
from  a  distance,"  such  as  is  seen  in  nerve-cells  when  the  neuraxon  is 
destroyed.  It  is  a  degeneration  which  affects  especially  the  body  of  the 
cell  and  not  so  much  the  nucleus;  hence  the  remarkable  power  of  recovery 
from  this  condition  which  so  many  people  show. 


392  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  diagnosis  of  the  disease  is  to  be  made  from  ordinary  suppurative 
meningitis,  from  acute  serous  meningitis  due  to  infection,  and  from 
acute  encephalitis.  In  most  cases  the  history  of  the  patient  is  quite 
sufficient  to  estabhsh  the  diagnosis.  The  symptoms  of  themselves  are 
almost  identical  with  those  of  ordinary  acute  suppurative  meningitis. 
The  only  distinctions  which  I  have  been  able  to  observe  are  that  in  sup- 
purative meningitis  there  is  more  fever,  there  is  less  of  the  low  delirium, 
hallucinations  are  rare,  and  there  is  an  earlier  and  more  profound  coma. 
In  other  words,  it  is  an  acuter  and  more  severe  malady  than  alcoholic 
meningitis.  The  absence  of  convulsions  and  paralysis  and  the  presence 
of  hypersesthesia,  rigidity,  and  contracted  pupils,  as  well  as  the  absence 
of  pyrexia,  are  usually  sufficient  to  distinguish  the  disorder  from  enceph- 
alitis or  encephalitis  complicated  by  alcoholic  meningitis.  Lumbar 
puncture  will  settle  the  diagnosis  and  often  prognosis.  The  cerebro- 
spinal fluid  is  usually  in  excess  and  under  great  pressure;  it  is  clear  and 
colorless,  unless  there  has  been  a  superimposed  infection  as  sometimes 
occurs,  when  evidence  of  inflammation  will  be  found. 

The  prognosis  is  bad  when  the  disease  has  become  well  developed  and 
when  decided  coma  and  rigidity  have  set  in.  A  prognostic  criterium 
which  I  have  long  used  and  which  is  fairly  accurate  is  this :  if  the  patient 
has  not  a  very  stiff  neck  and  back  he  will  get  well. 

The  treatment  of  the  disorder  should  be  instituted  at  the  very  be- 
ginning. If  there  are  still  any  relics  of  the  debauch,  as  shown  in  the 
condition  of  the  stomach  or  intestinal  tract,  the  stomach  should  be 
washed  out  and,  at  all  events,  a  thorough  purge  should  be  given.  The 
patient  should  then  be  fed  most  liberally  with  hot  milk  given  every  two 
hours;  beef  tea  and  an  egg  beaten  up  in  milk  may  also  be  given,  but  the 
condition  of  practical  starvation  on  the  part  of  the  patient  should  always 
be  borne  in  mind.  Stimulants  in  the  shape  of  whiskej^  should  not  be 
administered  if  it  is  possible  to  avoid  it,  but  strychnine  in  doses  of  one- 
sixtieth  of  a  grain  every  two  hours  is  often  useful.  An  ice  cap  may  be 
applied  to  the  head  and  at  times  leeches  or  large  blisters  seem  to  be  useful, 
applied  to  the  back  of  the  neck.  The  patient,  however,  should  not  be 
much  depleted.  Large  doses  of  ergot  have  been  recommended.  When 
he  becomes  comatose  it  means  that  the  ventricles  and  arachnoid  cavities 
are  becoming  filled  with  water.  At  this  time  tapping  the  spinal  cord  may 
be  tried.  I  have  done  this  in  a  number  of  cases  and  have  at  times  re- 
moved two  or  three  ounces  of  fluid  with  some  amelioration  of  the  symptoms 
and  never  any  bad  results,  but  I  have  never  seen  it  do  any  permanent  good. 

CEREBRAL  HYPERiEMIA  AND  AN.EMIA 

Active  Cerebral  Hyperaemia.- — The  circulation  of  the  blood  in  the 
brain  is  regulated  mainly  by  the  vasomotor  splanchnic  nerves,  a  rather 


DISEASES    OF    THE   BEAIN    AND    ITS    MEMBRANES  393 

clumsy  system  by  which  a  mass  of  blood  is  thrown  into  the  abdominal 
cavity,  or  pressed  out  of  it,  thereby  decreasing  or  increasing  the  cerebral 
flow.  In  addition  to  this,  the  cerebral  blood-vessels  have  a  nervous  supply 
which  probably  controls  the  finer  and  the  more  local  variations  in  calibre. 

The  total  amount  of  blood  in  the  cranial  cavity  is  always  about  the 
same.  There  can  be  no  cerebral  hypersemia,  therefore,  characterized 
by  a  large  increase  in  the  intra-cranial  content  of  blood.  But  the  flow 
of  blood  through  the  brain  may  be  very  much  increased  in  rapidity;  so 
that  the  amount  of  blood  flowing  through  the  brain  in  a  given  time  is 
greater  than  the  normal,  or  average. 

This  physiological  cerebral  hypera^mia  accompanies  conditions  of 
over-activity  and  over-stimulation  of  the  brain,  and  is  associated  with 
increase  in  mental  activity;  but  cerebral  hypersemia  is  here  a  consequence 
or  associated  phenomenon  rather  than  the  cause,  and  there  is  no  patho- 
logical condition  which  can  be,  strictly  speaking,  called  "cerebral  hy- 
persemia." 

Passive  or  venous  cerebral  hypercemia  occurs  when  there  is  some  block- 
ing of  the  venous  current  and  damming  back  of  the  blood.  Here  the 
venous  stasis  causes  an  increase  in  intra-cranial  pressure  and  an  anaemia 
of  the  capillaries.  The  blood  current  is  slowed-up  and  in  addition  to  that, 
the  proportion  of  venous  blood  to  arterial  is  increased.  The  blood  sup- 
ply is  not  of  as  good  quality  as  normal,  hence,  in  passive  hypersemia 
of  the  brain  there  may  be  symptoms.  They,  however,  are  usually  very 
much  like  those  of  cerebral  ansemia.  They  consist  in  a  sense  of  fullness 
of  the  head,  headache,  dizziness,  sometimes  faintness  and  there  may]  be 
dullness  and  drowsiness,  irritability  and  depression,  in  fact,  all  such 
symptoms  as  are  found  in  slowly  acting,  badly  nourished  or  toxic  brains. 

Cerebral  anaemia  is  a  more  definite  pathological  condition.  Acute 
ansemia  of  the  brain  occurs  as  the  result  of  severe  general  hemorrhage,  or 
of  sudden  intra-cranial  pressure  as  in  cerebral  hemorrhage,  and  of  acute 
serous  effusion.  It  may  be  caused  by  a  weak  and  diseased  heart.  It 
occurs  from  sudden  dilatation  and  paralysis  of  the  vaso-motor  splanchnic 
area,  and  it  probably  occurs  sometimes  in  cases  of  extreme  fright.  It  is 
caused  also  by  certain  toxic  conditions,  as  in  the  vaso-motor  paralysis 
of  chloroform  poisoning.  It  may  occur  in  conditions  of  impeded  circula- 
tion of  the  lungs  and  in  mechanical  obstruction  in  the  flow  of  blood  in 
the  neck. 

When  the  condition  is  of  acute  onset,  there  is  dilatation  of  the  pupils, 
respiration  deepens  and  is  irregular;  there  is  dizziness,  slowness  of  the 
heart  beat  and  rise  of  arterial  pressure.  This  is  followed  by  a  rapid  heart 
beat,  rise  of  arterial  pressure  and  finally  respiratory  paralysis. 

In  very  acute  ansemia,  such  as  is  caused  by  ligature  of  all  the  arteries 
carrying  blood  to  the  head  there  is  loss  of  consciousness  and  convulsions. 


394  DISEASES    OF    THE    NERVOUS    SYSTEM 

When  the  cerebral  anaemia  is  of  slow  onset  and  raore  or  less  chronic 
in  character,  the  symptoms  are  those  referred  to  in  large  measure  under 
the  head  of  "passive  hypersemia."  There  is  headache,  tinnitus,  vertigo, 
dullness,  drowsiness,  irritability,  insomnia  and  depression.  There  may 
be  dimness  of  vision  and  hearing,  and  muscular  weakness  and  the  general 
symptoms  of  a  poorly  acting  brain. 

As  a  matter  of  fact,  however,  it  is  probable  that  in  cerebral  anaemia 
these  symptoms  are  due  as  much  to  the  presence  of  toxic  elements  as  to 
the  insufficiency  of  blood. 

In  serious  forms  of  general  anaemia  and  even  in  the  most  severe  types 
of  pernicious  anaemia  no  very  marked  cerebral  symptoms  occur. 


CHAPTER  XVIII 

DISEASES  OF  THE  BRAIN 

These  diseases,  like  those  of  other  parts  of  the  nervous  system, 
consist  of  malformations,  vascular  disturbances,  inflammations,  soft- 
enings, hemorrhages,  degenerations  and  scleroses,  chronic  infections, 
tumors  and  functional  disorders. 

THE  INFLAMMATIONS  OF  THE  BRAIN 

The  important  forms  are  acute  suppurative  encephalitis,  acute  exu- 
dative forms  of  encephalitis,  chronic  meningo-encephaHtis  (general 
paresis)  and  multiple  sclerosis. 

ACUTE  SUPPURATIVE  ENCEPHALITIS 

{Abscess  of  the  Brain) 

Brain  abscess  is  a  suppurative  inflammation  which  affects  the  par- 
enchymatous and  other  structures  of  the  organ.  It  is  always  a  focal 
disease,  but  may  be  single  or  multiple. 

Etiology.' — The  primary  cause  of  all  forms  of  brain  abscess  is  practi- 
cally a  microbic  infection.  The  form  of  microbe,  its  mode  of  entrance, 
and  the  part  of  the  brain  attacked  vary  greatly.  The  predisposing  causes 
relate  chiefly  to  age  and  sex.  Brain  abscess  rarely  occurs  before  the  first 
year  or  after  the  fiftieth  year  of  life.  It  is  rather  frequent  in  young  people, 
and  occurs  on  the  whole  oftenest  between  the  ages  of  ten  and  thirty. 
Males  are  more  often  affected  than  females  in  the  ratio  of  about  three  to 
one.  The  exciting  causes  are  chiefly  disease  of  the  ear,  of  the  nose,^  and 
of  the  cranial  bones,  injuries,  remote  suppurative  processes,  and  septic 
and  other  infections.  Chronic  inflammation  of  the  middle  and  internal 
ear  is  the  most  common  cause  of  brain  abscess,  especially  when  that  dis- 
ease affects  the  tympanum  and  mastoid  cells.  Only  a  small  percentage 
of  abscesses  (about  8  per  cent.)  follow  acute  otitis  media.  This  is  the 
reason  more  cases  occur  in  adults.  Caries  of  the  ethmoid  and  nasal 
bones  and  of  the  orbital  cavity  leads  to  brain  abscesses  in  a  considerable 
proportion  of  cases.     After  chronic  ear  and  bone  diseases  injuries  are 

^  In  9,000  consecutive  autopsies  at  Guy's  Hospital  there  were  fifty-seven  brain 
abscesses  due  to  ear  diseases  and  one  due  to  nasal  disease  (Pitt). 

395 


396  DISEASES    OF    THE    NERVOUS    SYSTEM 

the  most  frequent  cause,  making  up  about  50  per  cent,  in  all.  The  injury 
may  be  a  compound  fracture  with  direct  infection  from  the  open  wound, 
or  the  abscess  may  be  the  result  of  ccntreccup  and  may  develop  in  a  part 
of  the  brain  opposite  to  that  which  was  injured,  or  the  abscess  may  de- 
velop below  the  point  injured,  there  being  apparently  healthy  tissus 
between  the  surface  of  the  brain  and  the  diseased  part.  These  abscesses 
develop  through  laceration  of  brain  tissue  and  subsequent  infection  of 
the  wound  with  organisms.  The  most  common  remote  suppurative 
processes  which  are  followed  by  brain  abscess  are  tuberculous  inflamma- 
tion of  the  lungs,  fetid  bronchitis,  and  empyema.  Brain  abscess  may 
develop,  however,  from  distant  points  of  suppuration  on  the  extremities 
or  in  almost  any  part  of  the  body.  General  sepsis  may  lead  to  the  pro- 
duction of  brain  abscess.  Among  the  infectious  fevers  which  are  compH- 
cated  with  brain  abscess  are  diphtheria,  typhoid  and  typhus  fevers,  ery- 
sipelas, small-pox,  the  grippe.  The  oidium  albicans  or  thrush  may  also 
be  a  cause.  Brain  tumors  sometimes  become  surrounded  by  a  suppura- 
tive encephalitis  or  may  break  down  with  the  formation  of  mixed  sup- 
purative and  neoplastic  tissue.  Tuberculous  tumors  are  most  frequently 
accompanied  by  suppurative  encephalitis. 

Symptoms. — Brain  abscesses  take  sometimes  an  acute  and  sometimes 
a  chronic  course.  In  acute  cases  the  symptoms  develop  rapidly  and  the 
disease  runs  its  course  in  a  few  days  or  weeks.  The  symptoms  come  under 
the  general  head  of  those  of  pressure,  those  of  poisoning  from  the  diseased 
focus,  and  local  symptoms  due  to  irritation  or  destruction  of  certain 
special  areas  of  the  brain.  The  pressure  symptoms  are  those  of  headache 
which  is  often  very  severe  and  persistent,  vomiting  which  is  quite  fre- 
quent, though  not  invariable,  vertigo,  and  a  condition  of  mental  dullness 
which  may  pass  into  a  delirium  ending  finally  in  coma.  Optic  neuritis 
often  occurs.  The  pupils  are  apt  to  be  irregular,  but  furnish  no  definite 
indications.  The  pulse  is  usually  slow,  ranging  from  60  to  70,  but  it 
varies  a  great  deal.  The  temperature  is  normal  or  subnormal,  as  a  rule, 
but  this  also  varies,  and  it  may  rise  several  degrees  above  normal,  always 
running  an  irregular  course.  The  blood  may  show  an  increase  in  leuko- 
cytes and  especially  of  the  polymorphs.  This  is  not  always  the  case, 
however,  and  absence  of  leukocytosis  does  not  exclude  abscess.  The 
toxic  symptoms  are  those  which  we  get  in  septic  poisoning;  namely, 
prostration,  irregular  fever,  emaciation,  anorexia,  and  such  mental  and 
sensory  disturbances  as  have  already  been  referred  to.  As  a  result  of 
local  irritation  or  destruction,  there  occur  convulsions,  paralysis,  aphasia, 
and  disorders  of  some  of  the  special  senses.  Convulsions  are  not  very 
common.  When  they  occur  they  are  generally  of  an  epileptic  character. 
The  paralysis  is  usually  in  the  form  of  hemiplegia.  The  cranial  nerves 
are  not  often  involved,  if  we  except  the  optic.     The  urine  is  said  to  show 


DISEASES    OF    THE   BRAIN  397 

a  diminution  in  chlorides  and  an  increase  in  phosphates.  The  patient 
dies  finally  in  coma  from  exhaustion. 

In  the  chronic  form  of  brain  abscess  the  symptoms  may  for  weeks, 
months,  or  years,  remain  practically  latent,  after  the  exciting  cause  has 
been  at  work  and  after  the  abscess  has  been  established.  The  patient 
during  this  latent  stage  may  suffer  from  headache,  vertigo,  mental 
irritability,  and  depression;  he  may  at  times  have  a  convulsive  attack. 
Occasionally  there  will  be  an  exacerbation  of  the  disease,  at  which  time 
he  suffers  from  intense  pain,  vomiting,  perhaps  delirium  or  a  convulsion. 
From  this  he  recovers  and  continues  in  a  fairly  good  state  of  health  again. 
After  a  variable  period,  usually  of  weeks  or  months,  the  terminal  stage 
sets  in.  This  terminal  stage  of  the  chronic  form  may  assume  very  much 
the  characters  of  the  acute  form  already  described.  In  other  cases  it 
shows  itself  by  a  sudden  apoplectic  or  epileptic  seizure  or  a  sudden  attack 
of  coma,  in  which  the  patient  sinks  and  rapidly  dies.  These  terminal 
phenomena  are  due  to  the  fact  that  the  abscess,  which  has  been  previously 
encysted  and  quiescent,  suddenly  breaks  into  a  lateral  ventricle  or  through 
the  surface  of  the  brain,  or  to  the  fact  that  a  hemorrhage  occurs  into  the 
abscess. 

Complications. — The  common  complications  of  brain  abscess  are  a 
phlebitis  of  the  superior  petrosal  and  lateral  sinuses  and  a  meningitis. 
The  phlebitis  accompanies  abscesses  that  are  caused  by  disease  of  the 
ear.  The  meningitis  may  be  caused  by  ear  disease,  but  more  frequently 
accompanies  abscesses  due  to  injury.  When  phlebitis  is  present  there 
will  be  found  an  oedema  about  the  ear  and  neck  and  a  hardness  of  the 
jugular  veins.  In  meningitis  there  is  apt  to  be  more  rigidity  of  the  neck, 
more  pain,  and  there  are  often  cranial-nerve  paralyses. 

Pathology. — Acute  suppurative  encephalitis  resembles  acute  suppura- 
tive myelitis  in  the  intimate  nature  of  the  changes  that  take  place.  There 
is  an  intense  congestion  of  the  part,  which  gives  it  a  reddened  appearance 
and  which  used  to  give  to  this  process  the  name  of  red  softening.  This 
condition,  however,  is  only  the  initial  stage  of  the  suppurative  inflamma- 
tion and  does  not  deserve  to  be  ranked  as  a  special  form  of  inflammatory 
process.  As  the  process  continues  the  parts  become  crowded  with  leuko- 
cytes and  infiltrated  with  inflammatory  exudate.  The  nerve-fibres  and 
cells  are  destroyed,  in  part  mechanically,  in  part  by  the  poisonous  influ- 
ence of  the  pyogenic  organisms.  The  nerve-cells  lose  their  normal  con- 
tours, swell  up,  and  disintegrate;  the  neuroglia  cells  absorb  the  broken- 
down  detritus  and  swell  up,  forming  what  are  known  as  granular  cor- 
puscles; the  leukocytes  increase  until  a  purulent  mass  is  formed.  The 
total  result  is  a  mixture  of  broken-down  nerve-fibres  and  cells,  leuko- 
cytes, and  granular  bodies.  Bacteriological  tests  show  the  presence  of 
various    pyogenic    microbes.     Usually    staphylococci    or    streptococci; 


398 


DISEASES    OF   THE    NERVOUS    SYSTEM 


rarely  the  pneumococcus.  The  abscess  thus  formed  varies  in  size  from 
1  cm.  to  6  or  8  cm.  in  diameter  (two-fifths  of  an  inch  to  three  inches). 
It  is  generally  somewhat  round,  and  if  the  case  is  chronic  a  fibrous  wall 
is  formed.  It  takes  from  three  to  four  weeks  for  such  a  wall  to  develop 
(Fig.  201).  Brain  abscesses  are  usually  single,  occasionally  there  are  two 
or  three.  In  some  conditions  they  are  multiple,  that  is  to  say,  there  may 
be  fifteen,  twenty,  or  more.  Multiple  brain  abscesses  are  always  small 
and  are  usually  due  to  pysemic  infection. 

Location. — Brain  abscesses  involve  the  cerebrum  oftener  than  the 
cerebellum,  in  the  proportion  of  about  four  to  one  (Barr) ;  two  to  one  (Le 


Fig.  201. — -Abscess  of  cerebellum. 


Fort  and  Lehmann).  They  occur  rather  oftener  in  the  right  cerebrum. 
They  are  very  rare  in  the  pons  and  medulla.  The  cerebral  lobes  oftenest 
affected  are  the  temporal  and  frontal.  In  the  cerebellum  it  is  the  lateral 
hemispheres  that  are  most  frequently  attacked.  The  seat  of  the  abscess 
has  important  relations  to  the  cause.  Abscesses  due  to  ear  disease  are 
almost  always  either  in  the  temporal  lobe  or  in  the  cerebellum.  If  the 
ear  disease  is  in  the  tympanum,  the  cerebrum  is  usually  the  seat  of  the 
abscess.  If  the  disease  is  in  the  mastoid  cells,  the  cerebellum  is  usually 
the  part  affected.  If  the  disease  is  in  the  labyrinth,  the  abscess  is  also 
more  apt  to  be  in  the  cerebellum.  This  distribution  of  the  seat  of  the 
disease  is  due  to  the  anatomical  relations  of  the  bony  parts  to  the  temporal 


DISEASES    OF    THE   BRAIN 


399 


lobe  and  cerebellum,  respectively.  Small  veins  from  the  temporal  lobe 
and  small  veins  from  the  tympanum  connect  with  the  superior  petrosal 
sinus,  and  thus  establish  a  pathway  of  infection.  Often  there  is  a  sinus 
thrombosis  and  inflammation.  Similarly  small  veins  from  the  cere- 
bellum and  the  mastoid  and  labyrinth  connect  with  the  lateral  sinus,  and 
here  too  a  phlebitis  may  be  established.  Brain  abscesses  due  to  injuries 
are  more  frequent  in  the  frontal  and  temporal  lobes.  What  are  known 
as  idiopathic  brain  abscesses — that  is,  those  which  arise  without  any 
known  cause — are  most  frequent  in  the  frontal  lobes.  This  is  because 
most  such  cases  are  due  to  an  unrecognized  affection  of  the  nasal  cavities 
and  ethmoid  bone.  Infection  from  the  nasal  and  ethmoid  cavities  may 
lead  to  sinus  thrombosis  also,  or  to  a  localized  purulent  meningitis,  some- 


FiG.  202. — Showing  the  points  where  the  trephine  is  usually  applied  and  the  relations 
of  the  sinus.     The  divisions  of  the  lines  indicate  quarter-inches.     (Lancet.) 


times  called  extra-cerebral  abscess.  Such  infections  sometimes  cause 
also  only  a  local  non-purulent  meningitis  involving  the  optic  nerves. 
Brain  abscesses  due  to  suppurative  processes  in  the  lungs  and  pleura  are 
probably  embolic;  and,  as  the  emboli  are  carried  up  into  the  middle 
cerebral  artery,  the  brain  abscesses  having  this  origin  are  situated  in  the 
field  supplied  by  this  artery.  In  children  under  ten,  in  whom  brain 
abscess  is  usually  due  to  ear  disease,  the  cerebellum  is  more  apt  to  be 
affected. 

Course. — Acute  abscesses  last  from  five  to  fourteen  days,  rarely  over 
thirty  days.  Traumatic  cases  run  the  shortest  course.  Chronic  ab- 
scesses may  have  a  latent  period  of  weeks,  months,  and  in  rare  cases  even 
one  or  two  years.     When  terminal  symptoms  come  on,  death  occurs  in  a 


400  DISEASES    OF    THE    NEEVOUS    SYSTEM 

few  days.  In  a  few  cases  brain  abscesses  have  been  spontaneously 
evacuated  through  the  nose.  Aside  from  this,  the  termination  is  always 
a  fatal  one  unless  surgical  interference  takes  place.  There  is  sometimes 
a  recurrence  of  the  abscess  after  an  operation. 

Prognosis. — The  outcome  of  brain  abscess  is  always  a  fatal  one  unless 
surgical  interference  takes  place.  There  is  sometimes  a  recurrence  of  the 
abscess  after  an  operation. 

Diagnosis. — The  diagnosis  of  brain  abscess  is  based  upon  the  history 
of  injury,  aural  or  nasal  disease,  or  remote  suppuration,  upon  the  general 
symptoms  of  sepsis,  upon  the  presence  of  headache,  vomiting,  slow  pulse, 
normal  or  subnormal  and  irregular  temperature,  a  local  tenderness  of  the 
scalp  and  rise  of  temperature  over  the  seat  of  the  lesion,  hebetude,  de- 
lirium, optic  neuritis,  rapid  wasting,  and  diminution  of  chlorides  in  the 
urine  and  leukocytosis  with  a  high  polymorph,  count.  Lumbar  puncture 
may  help  to  exclude  a  meningitis.  Puncture  of  the  brain  itself  has  been 
recommended,  and  it  may  be  tried  under  conditions  which  allow  prompt 
operation  if  indicated. 

The  diagnosis  of  the  location  of  the  abscess  is  based  upon  the  history 
of  its  cause,  whether  from  injury,  ear  disease,  emboli  from  the  lungs,  or 
nasal  disease;  also  upon  the  presence  of  hemiplegia,  local  convulsions, 
tenderness  and  rise  of  temperature  of  a  certain  area  of  the  scalp.  As 
brain  abscesses  are  apt  to  affect  latent  regions  like  the  temporal  and 
frontal  lobes,  local  diagnosis  is  often  difficult.  The  diagnosis  must  be 
made  from  tumors  of  the  brain,  meningitis,  and  phlebitis  of  the  sinuses. 
The  differential  points  are  given  under  the  heads  of  the  diseases  mentioned. 
In  some  cases  of  otitis  media  symptoms  of  abscess  occur,  but  there  is  an 
exquisite  superficial  tenderness  limited  to  the  region  of  the  trigeminus. 
These  cases  recover  and  are  perhaps  due  to  a  dural  congestion  (Gushing). 
Sometimes,  also,  in  otitis  symptoms  of  the  acute  serous  meningitis  of 
Quincke  occur,  which  are  reheved  by  lumbar  puncture.  Sometimes 
with  nasal  disease  there  maj^  develop  optic  neuritis,  headache  and  other 
symptoms  of  brain  involvement,  but  no  general  symptoms,  and  no  symp- 
toms of  serious  brain  irritation.  These  are  cases  of  localized  frontal 
meningitis  and  they  get  well. 

Treatment. — The  actual  treatment  of  a  brain  abscess  after  it  has  de- 
veloped is,  as  already  stated,  exclusively  a  surgical  one.  The  successes 
so  far  have  not  been  very  great,  but  they  have  been  sufficient  to  justify 
operation  and  to  furnish  greater  hope  for  the  future,  when  a  more  exact 
diagnosis  can  be  made  and  a  wider  surgical  experience  has  been  obtained. 
According  to  Gushing,  the  percentage  of  recoveries  now  is  about  fifty. 
The  accompanying  figure  shows  the  points  to  be  located  in  trephining  for 
abscess  from  ear  disease.  Something  is  due  to  the  patient  in  the  way  of 
prevention,  especially  in  cases  of  persons  who  have  chronic  aural  or 


DISEASES    OF   THE   BRAIN  401 

nasal  disease  with  carious  processes.     These  should  be  carefully  watched 
and  treated. 

ACUTE  NON-SUPPURATIVE  ENCEPHALITIS 

{Hemorrhagic  Encephalitis,  Hemorrhagic  Polioencephalitis) 

Acute  non-suppurative  encephalitis  is  an  exudative  and  sometimes 
hemorrhagic  inflammation  of  the  brain,  characterized  by  symptoms  of 
general  infection  or  toxaemia,  of  severe  cerebral  irritation,  and  the  signs 
of  local  cerebral  lesion.  It  is  sometimes  spoken  of  as  a  non-suppurative 
encephalitis  and  as  a  curable  encephalitis.  The  disease  occurs  as  one 
form  of  the  infection  when  an  epidemic  of  anterior  poliomyelitis  occurs. 
In  some  of  its  forms,  it  is  probably  a  rather  common  affection,  complicat- 
ing especially  the  acute  infectious  fevers  of  childhood  and  of  influenza. 

The  disease  then  may  be  grouped  in  the  following  manner: 


Acute  non-suppurative 
encephalitis. 


1.  Heine  Medin  type  of  encephalitis  due  to  the  microbic 
infection  which  causes  infantile  paralysis.  It  is  the 
encephalitic  expression  of  an  infantile  paralysis 
infection. 

2.  Acute  encephalitis,  due  to  various  other  infections. 

3.  Polioencephalitis  superior  and  inferior,  due  to  influ- 
enzal and  other  infections. 


1.  When  the  inflammation  is  due  to  the  poliomyelitic  infection  it 
occurs  as  a  complication  of  the  myelitis,  as  in  Landry's  paralysis;  or  it 
may  occur  as  a  separate  focal  lesion.  Such  cases  have  been  noted  in 
epidemics.     Fortunately  the  complication  is  rare. 

2.  The  ordinary  type  occurs  rather  more  frequently  in  children,  and 
a  special  children's  type  has  been  described.  It  attacks  the  cerebral 
hemispheres,  sometimes  the  cortical  gray  matter  alone,  very  rarely  the 
cerebellum. 

3.  The  mid-brain,  pontine  and  bulbar  forms  are  seen  in  the  adults, 
most  frequently  in  association  with  alcoholism  and  influenzal  infections. 

Etiology. — -The  disease  is  caused  by  the  same  infection  as  that  of 
epidemic  poliomyelitis;  by  other  acute  infections,  especially  those  of 
influenza,  of  the  fevers  of  childhood,  of  otitis  media,  and  other  nearby 
infected  centres;  it  is  one  of  the  results  and  complications  of  serious 
alcoholism.  It  occurs  most  often  in  the  young — except  in  Type  3 
caused  by  alcohol  and  influenza.  In  some  cases,  trauma,  when  associated 
with  some  slight  infection  and  perhaps  laceration  of  the  brain,  causes  it. 
Encephalitis  has  been  known  to  follow  a  malignant  endocarditis,  and  in 
connection  with  the  infections  of  the  puerperal  state. 


402  DISEASES    OF    THE    NERVOUS    SYSTEM 

Symptoms. — Symptoms  of  the  disease,  when  it  affects  the  medulla  or 
mid-brain  (Type  No.  3),  are  described  under  the  heads  of  acute  bulbar 
palsy  and  acute  ophthahrioplegia.  When  the  disease  attacks  the  hemi- 
spheres, it  begins,  as  in  most  of  the  cases,  rather  suddenly  and  without 
notable  premonitory  symptoms.  The  patient  is  seized  by  headache 
followed  by  fever  sometimes  reaching  105°F.  This  may  be  associated 
with  vertigo,  vomiting,  photophobia  and  delirium.  In  children  there  may 
be  convulsions.  The  symptoms  of  irritation  disappear  and  are  followed 
by  a  condition  of  semicoma  or  stupor.  The  patient  can  generally  be 
partly  aroused,  and  he  does  not  usually  have  the  stiff  neck  or  the  small 
pupils  of  meningitis.  The  respirations  are  shallow  and  frequent,  the  pulse 
is  rapid  and  feeble.  As  the  disease  progresses,  the  deep  reflexes  are  dimin- 
ished and  later  the  sphincters  may  be  involved.  After  the  patient  has 
lain  in  a  semicomatose  condition  for  several  days,  he  may  become  less 
stupid  and  more  irritable  and  restless;  or  after  two  or  three  weeks  of 
comparative  stupor  he  may  begin  gradually  to  improve  and,  in  a  few 
weeks  more,  convalescence  takes  place,  leaving  him  well  or  with  some 
motor  or  mental  defect. 

In  some  cases  an  epileptic  convulsion  may  occur  in  the  early  part  of 
the  disease.  Again,  as  the  disease  develops,  aphasia  and  paralysis  of  the 
arm  or  leg,  or  hemiplegia,  may  appear.  In  accordance  with  the  location 
of  the  inflammation,  the  patient  may  have  disturbances  in  the  motor 
sphere,  or  he  may  have  hemianopsia,  hemiataxia,  or  disturbance  of  the 
cranial  nerves,  such  as  nystagmus,  or  eye  palsy,  or  difficulty  in  speech 
and  deglutition.  Children  may  be  left  with  a  mental  defect,  and  prob- 
ably mild  attacks  of  this  disease  are  often  the  cause  of  such  defects,  or  of 
epilepsies,  attributed,  perhaps,  to  an  ordinary  infective  fever.  An  optic 
neuritis  may  also  occur. 

Course  and  Prognosis. — -The  disease  is  always  serious  but  is  not  by 
any  means  always  fatal.  It  may  in  its  milder  form  run  a  course  of  two 
or  three  weeks,  the  patient  gradually  coming  out  of  his  stupor  and  making 
a  slow  recovery.  In  other  cases  the  coma  continues  to  deepen  and  the 
patient  dies  of  exhaustion,  and  in  still  other  cases  the  disease  passes  into 
a  chronic  state  in  which  he  lingers  for  weeks  and  even  months. 

Diagnosis. — -The  Heine-Medin  tj'^pe  of  encephalitis  may  be  suspected 
if  the  symptoms  develop  in  the  course  of  an  epidemic  of  poliomyelitis. 
The  third  or  alcoholic  and  influenzal  type  of  the  disease  occurs  in  adults. 
The  second  or  common  type  is  seen  oftenest  in  children  and  is  probably 
often  mistaken  for  meningitis.  It  is  to  be  differentiated  from  this  by  the 
sudden  onset  with  coma,  the  absence  of  projectile  vomiting,  and  of  pinhole 
pupils,  stiff  neck,  hypersesthesia,  and  rigidity  of  the  limbs.  The  presence 
of  hemiplegia  or  local  paralysis,  or  the  occurrence  of  an  epileptoid  attack 
would  point  to  encephalitis.     The  previous  occurrence  of  an  attack  of 


DISEASES    OF   THE   BRAIN  403 

grippe  in  the  young,  or  of  exposure  to  the  sun  or  acute  alcoholism  in  the 
adult  would  lead  to  the  probability  of  an  encephalitis.  By  the  help  of 
lumbar  puncture  fluid  can  be  withdrawn  from  the  spinal  sac,  and  exami- 
nation of  it  will  exclude  meningitis. 

Pathological  Anatomy. — The  pathological  process  underlying  this 
disease  consists  of  an  acute  inflammation  with  intense  congestion  and 
numerous  small  hemorrhages  and  capillary  emboli.  There  is  some  hem- 
orrhagic exudation  as  well  as  infiltration  of  leukocytes,  with  a  certain 
amount  of  softening  of  the  cerebral  tissue  in  the  neighborhood.  The  parts 
most  frequently  affected  are  variously  stated  to  be  the  frontal  and  occip- 
ital lobes,  the  central  convolutions,  the  semi-ovale,  the  temporal  lobes, 
the  base  of  the  brain,  and  the  corpus  striatum.  In  four  cases  which  I 
have  examined,  the  process  was  in  the  temporal  lobes,  the  parietal  lobule, 
the  mid-brain  and  the  corpus  striatum.  It  has  been  known  to  affect 
the  cerebellum.  If  the  process  is  a  mild  one,  the  hemorrhage  and  exu- 
date are  absorbed,  and  the  injured  brain  tissue  is  gradually  replaced  by 
connective  and  neuroglia  tissue.  In  this  way  small  foci  of  sclerotic  tissue 
are  formed  and  the  patient  may  afterward  suffer  from  symptoms  due  to 
this  condition.  In  the  severer  cases  the  softening  becomes  more  exten- 
sive, larger  hemorrhages  occur,  and  in  one  case  I  have  seen  a  massive 
apoplexy  as  the  terminal  stage. 

Treatment. — ^The  patient  should  be  kept  quietly  in  bed  and  should 
be  given  an  active  purge.  Calomel  is  usually  employed,  but  croton  oil 
has  seemed  to  me  to  be  much  more  efficient  as  an  eliminative  and  counter- 
irritant.  The  kidneys  should  be  kept  active,  an  ice  cap  placed  upon  the 
head,  and  leeches  placed  at  the  back  of  the  neck.  Urotropin  may  be 
given.  The  treatment  after  this  can  be  only  that  of  elimination,  seda- 
tion and  support.  If  the  patient  is  stuporous  and  has  a  high  fever  small 
doses  of  aconite  should  be  given.  If  he  is  asthenic,  he  should  receive 
strychnine.  The  nourishment  should  be  carefully  attended  to  and,  if 
he  suffers  pain,  he  should  have  morphine.  Chloral  and  bromide  seem 
to  be  the  most  efficient  agents  for  relieving  the  restlessness  and  insomnia. 

GENERAL  PARESIS 

{General  Paralysis  of  the  Insane — Dementia  Paralytica) 

General  paresis  is  a  disease  of  the  brain  characterized  clinically  by 
peculiar  associated  physical  and  mental  disturbances,  which  end  eventu- 
ally and  usually  in  general  paralysis  and  mental  deterioration;  anatom- 
ically it  is  characterized  by  a  syphilitic  parenchymatous  meningo- 
encephalitis. The  disease  cannot  always  be  distinguished  clinically  from 
meningo-vascular  syphilis. 

Etiology. — -Paresis,  is  a  disease  of  modern  civilization  and  of  syphiliza- 
tion.     It  was  a  medical  curiosity  a  hundred  years  ago;  now  it  is  extremely 


404  DISEASES    OF   THE    NERVOUS    SYSTEM 

frequent  in  our  asylums,  in  neurological  clinics,  and  in  private  practice, 
and  it  has  become  much  more  common  of  late  years  partly  because  it  is 
more  frequently  recognized.  It  is  found  in  all  the  civilized  races  of 
Europe  and  America.  It  affects  even  the  inferior  races  living  among 
civilized  people,  and  is  found,  for  example,  among  the  negroes  of  the 
United  States,  affecting  especially  the  negresses  (Dieffenbach) . 

It  is  said  to  be  rare  among  Chinese  and  Japanese  and  in  Moham- 
medan countries  even  where  syphilis  prevails.  It  is  more  frequent  in 
countries  where  social  conditions  lead  to  the  spread  of  syphilis.  It  is 
rare,  as  a  rule,  in  rural  communities  as  compared  with  cities.  However, 
in  countries  where  there  is  enforced  military  training  and  a  period  of 
barrack  life,  the  disease  becomes  prevalent  in  the  country.  It  occurs 
oftener  in  men  than  women.  In  my  private  practice  the  ratio  is  about 
10  to  1 ;  in  hospital  practice  it  is  about  3  or  4  to  1.  It  occurs  oftener  in  the 
married  absolutely  but  not  relatively.  It  is  a  disease  of  middle  life,  most 
cases  occurring  between  thirty  and  fifty;  and  few  cases  develop  before 
or  after  these  ages.  The  women  when  attacked  are  a  little  younger  than 
the  men. 

Neuropathic  races  and  neuropathic  persons  are  more  susceptible  to 
the  disease.  Paresis  is  sometimes  (0.03  per  cent.)  directly  transmitted. 
It  then  appears  between  the  ages  of  ten  and  twenty  and  is  known  as 
juvenile  paresis.  In  this  form  males  and  females  are  about  equally 
affected. 

Occupation  is  a  predisposing  cause  in  just  about  the  proportion  with 
which  the  occupation  leads  to  exposure  to  syphilis.  In  Europe  it  is  very 
frequent  among  military  officers  in  some  countries  and  it  is  very  rare 
among  the  Catholic  clergy. 

The  excessive  use  of  alcohol,  excessive  mental  exertion,  if  combined 
with  emotional  strain  and  excitement,  sexual  excesses  and  abuse  are 
predisposing  causes.  A  certain  popular  idea  that  the  disease  is  the  result 
of  perverted  sexual  indulgence  is  not  correct.  It  has  now  become 
firmly  established  that  paresis  is  always  due  to  a  syphilitic  infection, 
which  leads  to  a  parenchymatous  degeneration  of  cerebral  neurons;  just 
as  tabes  is  due  to  a  similar  affection  of  the  spinal  neurons.  It  occurs 
in  about  1  to  2  per  cent,  of  all  luetics  and  makes  up  about  10  per  cent, 
of  our  asylum  population.  It  comes  on  oftenest  between  the  tenth  and 
twentieth  year  after  the  infection. 

Symptoms  (Prodromata) .— Paresis  is  sometimes  preceded  by  a  pro- 
dromal period  which  may  last  for  four  or  five  years,  more  often  perhaps 
a  year.  During  this  time  the  patients  suffer  from  symptoms  that  re- 
semble somewhat  those  of  neurasthenia,  sometimes  those  of  a  mild  anxiety 
psychosis.  The  patient  shows  a  change  in  character.  He  is  more  irrita- 
ble, less  able  to  concentrate,  has  some  memory  defect,  and  is  less  efficient 


DISEASES    OF    THE   BEAIN  405 

in  his  work.  He  has  headache,  insomnia  and  cerebral  and  spinal  dys- 
sesthesias,  and  parsesthesias.  He  worries  about  himself  and  is  termed  hy- 
pochondriacal. At  this  stage  he  often  has  quite  clear  insight  and  appre- 
ciates his  danger.  But  unlike  cases  of  true  neurasthenia  he  cannot  do 
efficient  work,  though  he  may  wish  to  do  so.  If  there  is  a  little  tempera- 
mental elation  he  may  work  unwisely  and  foolishly.  It  sometimes  hap- 
pens that  the  peculiarities  of  mind  and  conduct  are  so  slight  that,  it  is 
only  in  retrospect,  and  after  serious  conditions  develop  that  the  family 
remember  the  early  changes. 

In  more  advanced  cases  the  patient  may  suddenly  develop  a  con- 
vulsion, or  some  change  in  the  pupils  and  reflexes  may  appear. 

Physical  examination  may  not  reveal  any  objective  changes,  except 
that  his  fluids  may  show  positive  reaction  to  the  Wassermann  and  other 
luetic  tests,  but  this  is  rather  easily  controlled  by  treatment.  Such 
patients  under  active  treatment  may  get  well;  but  if  the  trouble  is  not 
recognized,  some  form  of  cerebral  syphilis  eventually  develops.  Even 
if  this  luetic  neurasthenia  progresses  till  some  characteristic  mental  and 
physical  symptoms  of  paresis  or  tabo-paresis,  or  meningeal  syphilis 
develop,  the  patient  may  get  well  or  at  least  secure  a  complete  remission. 
The  preparetic  condition  is  a  curable  one. 

But  besides  these  neurasthenic  and  anxiety  prodromata,  paresis  may 
be  preceded  by  a  distinct  functional  psychosis.  This  takes  the  form 
oftenest  of  a  luetic  melancholia,  more  rarely  of  a  mania.  The  patient 
may  and  generally  does  emerge  from  this  and  he  may  then  remain  well, 
but  more  often  unless  treatment  is  unusually  effective,  he  begins  to  de- 
velop the  characteristic  signs  of  general  paresis.  Very  rarely  paresis 
comes  on  suddenly  like  an  explosion. 

Finally  and  not  rarely  paresis  is  preceded  by  distinct  symptoms  of 
cerebral  or  cerebrospinal  meningeal  syphilis,  or  by  a  tabes  dorsahs. 

Thus  paresis  is  approached  in  four  different  ways,  clinically  speaking : 

1.  By  a  luetic  neurasthenia,  or  anxiety  psychosis. 

2.  By  a  luetic  melancholia  or  mania. 

3.  By  a  meningeal  cerebral  or  a  spinal  syphilis. 

4.  In  a  gradual  or  explosive  manner. 

General  paresis  is  classified  in  various  and  numerous  ways.  Many 
descriptions  have  been  based  on  a  study  of  custodial  and  more  or  less 
advanced  cases. 

The  description  and  classification  I  give  are  based  largely  on  a  per- 
sonal study  of  cases  as  I  have  seen  them  develop  and  pass  into  hospital 
conditions  or  into  states  of  improvement  and  remission.  The  various, 
phases  of  advanced  paresis  have  little  practical  interest. 

The  disease  develops  in 

1.  An  excited  form. 


406  DISEASES    OF    THE    NERVOUS    SYSTEM 

2.  A  depressed  form. 

3.  With  quiet  dementia. 

4.  In  an  explosive  form. 

These  various  types  may  change  in  the  course  of  the  disease. 

In  my  experience  about  one-third  are  at  first  seriously  depressed,  less 
than  a  third  maniacal  and  more  than  a  third  pass  with  perhaps  some 
slight  excitement  or  delusional  activity  into  a  progressive  dementia; 
that  is  to  say,  unless  the  course  is  modified  by  treatment.  In  all  cases 
some  meningeal  symptoms  may  be  present. 

Symptoms  of  Onset :  Active  Type.- — In  the  first  type  of  cases  the  pa- 
tient begins  by  showing  unusual  irritability  of  temper;  trivial  things  an- 
noy him,  and  his  bad  humor  and  change  of  disposition  become  notice- 
able in  his  family  relations  and  in  his  business.  He  is  fretful;  complains 
of  being  easily  fatigued ;  loses  interest  in  his  affairs,  and  is  unable  to  fix 
his  attention  for  any  length  of  time  upon  them.  He  makes  occasional  mis- 
takes of  judgment,  and  does  some  extravagant  or  foolish  thing  in  the  way 
of  purchasing  or  selling.  He  is  totally  lacking  in  insight.  This  condition 
of  irritability  is  followed  by  one  of  great  mental  exaltation.  The  patient 
becomes  very  happy  and  cheerful  and  confident;  he  feels  better  than  he 
ever  did  before  in  his  life.  He  talks  excessively,  and  is  effusive  and 
j  ocose  when  he  used  to  be  sober  and  reserved.  He  develops  great  schemes 
for  the  future,  he  lavishes  money  uselessly  in  making  presents  to  his 
family  and  friends,  or  in  some  extraordinary  business  venture,  and 
imagines  himself  possessed  of  immense  wealth  or  great  power.  He  has, 
in  other  words,  delusions  of  grandeur,  or  megalomania.  This  condition 
of  exaltation  is  interrupted  by  outbursts  of  violence,  especially  if  it  leads 
him  to  indulge  in  drink,  as  is  often  the  case.  In  the  course  of  three  or 
four  months  the  symptoms  become  so  marked  that  the  family  recognize 
the  seriousness  of  his  state,  and  he  is  confined  in  some  institution  where 
he  can  do  himself  and  others  no  harm.  Under  institutional  regime  he 
now  becomes  somewhat  more  quiet;  his  exaltation  softens  down.  His 
symptoms  may  even  remit,  and  for  a  time  he  becomes  nearly  or  quite 
rational.  But  after  some  months  he  begins  to  show  distinct  signs  of 
dementia;  the  memory  becomes  weak,  he  forgets  recent  events,  mislays 
things,  makes  mistakes  in  his  accounts,  is  unable  to  add  correctly;  he  can- 
not write  a  letter  coherently,  or  if  he  does  there  are  mistakes  in  spelling 
and  elisions  of  letters. 

During  or  before  the  exaltation  there  gradually  appear  physical  symp- 
toms which  are  very  characteristic.  The  patient's  hands  become  tremulous, 
and  his  handwriting  is  so  affected  that  his  signature  often  cannot  be 
recognized.  There  is  distinct  and  decided  facial  tremor,  particularly 
apparent  if  the  patient  is  made  to  close  the  eyes  and  stretch  the  muscles 
of  the  lips  so  as  to  show  the  teeth. 


DISEASES    OF    THE   BRAIN  407 

There  is  marked  tremor  of  the  tongue,  all  this  tremulousness  being 
much  more  exaggerated  than  is  seen  in  other  diseases,  except  occasion- 
ally in  acute  alcoholism.  The  speech  becomes  stuttering  and  thick, 
and  he  cannot  pronounce  long  words  clearly.  On  examination  of  the 
reflexes  it  is  usually  found  that  the  knee-jerks  are  exaggerated.  The 
pupils  are  almost  always  uneven  and,  as  a  rule,  react  badly  to  light  though 
fairly  well  to  accommodation,  showing,  in  other  words,  the  Argyll- 
Robertson  pupil;  sometimes  they  do  not  react  either  to  light  or  accom- 
modation.    The  fundus  oculi  is  normal. 

There  is  an  early  and  decided  weakness  of  the  sexual  function.  The 
bladder  may  also  become  weak.  The  appetite  and  vegetative  organs 
remain  in  fairly  good  condition.  The  patient  often  suffers  from  per- 
sistent insomnia.  During  this  time  he  also  has  occasionally  vertiginous, 
syncopal,  or  apoplectiform  attacks.  In  the  latter  he  falls  down  and 
perhaps  has  hemiplegia  lasting  for  a  few  days  or  a  few  weeks.  An  epileptic 
convulsion  may  occur. 

In  some  cases  the  knee-jerks  are  abolished,  and  there  is  some  ataxia 
and  evidence  of  a  posterior  sclerosis.  The  general  muscular  power  is 
much  diminished,  and  the  patient  is  unable  to  take  long  walks  or  do  any 
great  amount  of  physical  exercise. 

In  the  second  stage  the  most  striking  feature  is  the  gradual  onset  of 
dementia.  The  patient  now  becomes  more  quiet  and  is  incHned  to  sleep 
during  the  daytime.  He  takes  little  interest  in  affairs  about  him,  is 
extremely  forgetful,  and  is  often  unable  to  recognize  even  his  intimate 
friends.  He  no  longer  knows  the  day  of  the  month  nor  the  year,  and 
cannot  tell  one  anything  about  current  events  of  the  day.  He  becomes 
gradually  careless  about  his  person,  and  has  to  be  watched  while  at  his 
meals  lest  he  spill  food  on  his  clothes,  and  at  the  toilet  lest  he  soil  him- 
self.    Finally,  he  needs  to  be  cared  for  as  if  he  were  a  child. 

At  this  late  period,  again,  attacks  of  an  apoplectiform  character  may 
come  on,  leaving  him  temporarily  or  perhaps  permanently  hemiplegic. 
His  appetite  often  continues  good,  sometimes  voracious,  and  he  may  gain 
flesh.  He  is  apt  at  this  time  to  have  periods  of  excitement  in  which 
he  has  delusions  of  persecution,  or  he  may  have  some  slight  delusions 
of  grandeur.  One  patient  of  mine  used  to  weigh  himself  every  day  and 
think  he  was  gaining  ten  pounds  each  time.  He  kept  on  till  he  thought 
he  weighed  nine  hundred  pounds. 

In  the  last  scene  of  all  he  becomes  bedridden  and  helpless,  terminal 
febrile  attacks  occur,  and  he  finally  dies  of  exhaustion.  The  somatic 
symptoms  during  this  last  period  consist  of  increased  tremor,  disturb- 
ances of  speech,  and  gradual  muscular  weakness  until  the  patient  be- 
comes helpless. 

The  average  duration  of  the  disease  is  about  three  years.     There 


408  DISEASES    OF   THE    NERVOUS   SYSTEM 

are  some  acute,  galloping  forms  in  which  the  patient  dies  within  a  year, 
and  there  are  some  cases  in  which  the  patient  reaches  a  stage  of  partial 
or  complete  dementia  and  remains  in  this  condition  for  ten  or  fifteen 
years. 

The  Depressed  Type. — In  this  form  the  disease  begins  with  symptoms 
resembling  those  of  neurasthenia  and  hypochondriasis.  The  patient 
complains  of  disagreeable  sensations  about  his  head,  hemicrania,  pain 
in  his  limbs  and  back,  inability  to  sleep,  disorders  of  the  stomach,  and 
vague  sensations  of  discomfort  and  oppression  which  he  is  unable  dis- 
tinctly to  describe.  These  are  the  patients  who  are  often  treated  as 
neurasthenics  for  a  long  time,  and  at  first  show  hardly  any  physical  or 
mental  symptoms  suggestive  of  the  real  trouble.  Careful  examination, 
now,  however,  will  show  some  objective  physical  changes  including  a 
positive  serological  formula. 

Now  evidences  of  mental  disturbances  appear,  and  they  are  mostly 
those  of  dementia  with  perhaps  delusions  of  persecutions  and  suspicion. 
These  delusions  may  be  accompanied  by  occasional  outbreaks  of  excite- 
ment and  violence,  but  the  paretic  is  rarely  homicidal  and,  it  may  be 
added,  rarely  suicidal,  except  when  he  has  distinctly  a  melancholia.  After 
dementia  has  set  in,  the  physical  symptoms  of  tremor,  scanning  speech, 
and  tremulous  handwriting  all  become  noticeable,  and  the  final  stage 
resembles  that  of  the  other  form. 

Dementing  Type. — In  a  third  type  there  is  a  primary  dementia. 
The  disease  begins  without  any  excitement  or  any  special  depression, 
with  symptoms  of  forgetfulness,  lack  of  attention  to  business,  and 
incapacity  to  do  work.  The  patient  makes  mistakes  in  his  calculations, 
mislays  and  forgets  things,  and  soon  is  found  by  his  employer  to  be  of 
no  use.  He  is  often  good-natured,  not  unhappy,  and  without  distinct 
delusions  of  any  kind.  The  somatic  symptoms  of  tremor,  fixed  pupils, 
and  exaggerated  reflexes  may  appear,  but  sometimes  are  entirely  absent. 
Scanning  speech  is  not  always  present,  or  comes  on  late. 

Tabo-paresis. — Some  symptoms  of  tabes  are  present  in  almost  10 
per  cent,  of  paresis.  It  is  the  paresis  that  is  the  early,  dominant  and 
important  factor;  for  tabo-paresis  is  really  and  practically  paresis. 
The  tabetic  symptoms  are  of  the  minor  kind:  Argyll-Robertson  pupil, 
lightning  pains,  loss  of  knee-jerk,  some  hypotonia  and  more  rarely  some 
ataxia.  When  tabes  becomes  fully  and  first  developed,  paresis  rarely 
appears  (3  to  5  per  cent,  of  cases). 

Meningo-vascular  or  Pseudo-paresis. — There  are  some  cases  of 
paresis  in  which  symptoms  of  exudative  syphilis  introduce  and  accompany 
the  disease.  The  patient  has  at  first  eye  palsies  or  attacks  of  hemiplegia 
with  intense  headache  followed  by  convulsions.  It  is  recognized  that 
he  has  a  syphilitic  exudate  pressing  upon  some  part  of  the  brain,  either 


DISEASES    OF    THE   BEAIN 


409 


the  base  or  the  convexity,  usually  the  former.  Under  proper  treatment, 
this  resolves  and  he  gets  over  the  paralysis  and  the  seizures,  but  it  is  now 
found  that  his  mind  is  slightly  affected.  He  has  no  delusions  perhaps, 
and  no  immediate  exaltation,  but  his  memory  is  impaired,  judgment 
weakened,  his  emotional  condition  is  one  of  excitability,  and  he  has  to 
give  up  business  and  live  a  quiet,  inactive  life.  If  he  does  this,  in  some 
cases  the  disease  becomes  arrested,  and  he  remains  fairly  well  for  a 
number  of  years.  Cases  of  apparent  recovery  have  been  reported,  but 
unless  treatment  controls  the  situation,  dementia  finally  sets  in.  In 
these  cases  there  is  both  a  parenchymatous  and  a  meningeal  syphilis. 


>^/ 


Fig.  203. — Left  hemisphere  in  a  case  of  general  paresis.  The  praifontal  area  of 
higher  association  is  grossly  wasted.  The  psychomotor  area  shows  some  but  much 
less  waiting.  The  temporal,  parietal  and  insular  regions  of  associations  are  acutely 
changed.  The  after  part  of  the  temporal  region  of  association  and  the  anterior  part 
of  the  parietal  show  less  acute  change  and  more  wasting.  The  visual  center  and  the 
visuopsychic  cortex  around  it  are  intact.     (Bolton.) 

Alcoholic  Pseudo-paresis. — Persons  who  have  for  long  periods  of 
time  continuously  and  excessively  indulged  in  alcohol  may  develop, 
and  generally  do,  a  condition  of  mental  weakness  which  to  a  certain 
extent  simulates  paresis.  If  these  patients  have  not  had  syphilis, 
however,  it  is  not  a  true  paresis.  The  patients  become  weak-minded, 
feeble  in  judgment,  poor  in  memory,  their  moral  instincts  get  out  of 
control,  and  acts  of  extraordinary  selfishness,  bestiality,  and  besotted- 
ness  are  manifest.  They  gradually  become  more  enfeebled,  and  finally 
enter  a  condition  of  dementia  if  they  are  not  carried  off  by  some  in- 
tercurrent disease,  as  is  often  the  case.  These  cases,  however,  do  not 
present  the  physical  symptoms  of  paresis.  They  do  not  have  the 
speech  disturbances,  the  paralyses,  or  the  apoplectiform  seizures   that 


410 


DISEASES    OF   THE    NERVOUS    SYSTEM 


characterize  the  true  disease,  and  if  they  can  be  kept  from  alcohol  they 
may  remain  in  a  state  of  partial  dementia  for  many  years. 

Diagnosis. — The  diagnosis  is  based  on  the  history  of  syphilis,  the 
positive  serology,  the  facial  and  tongue  tremor,  irregular  and  rigid  pupils, 
exaggerated  or  irregular  knee-jerks,  the  disturbance  of  speech,  weakness 
of  memory,  loss  of  power  to  work,  irritability  and  change  of  character, 
change  in  the  handwriting,  and  presence  of  convulsive  or  apoplectiform 
attacks.     Examination  of  the  cerebrospinal  fluid  and  blood  shows  serum 


Fig.  204. — Early  general  paresis.  A  small  cortical  artery  is  shown  with  a  begin- 
ning injection  of  round  and  plasma  cells;  dying  pyramidal  cells  are  also  to  be  seen 
(X320).     (Bolton.) 

Wassermann  +  ,  cerebrospinal  fluid,  Wassermann  +  ,  cells  per  cubic  milli- 
metre  +  +  ,  globulin +  ,  colloidal  gold+  (see  table,  page  412). 

Pathological  Anatomy. — The  dura  mater  is  adherent  to  the  calvarium 
in  places  or  throughout.  In  old  cases  there  is  sometimes  a  pachy- 
meningitis interna  with  hematoma.  The  pia  mater  is  cloudy  and 
thickened,  especially  over  the  frontal  and  parietal  regions,  less  on  the 
base  and  never  over  the  occipital  lobes.  The  brain  is  atrophic  in  old 
cases,  with  shrunken  convolutions  and  local  areas  where  the  brain  has 
especially  atrophied.  The  ventricles  are  dilated  and  show  a  granular 
surface.  The  loss  of  brain  weight  averages  about  five  ounces  and  is  most 
in  the  frontal  lobes.  Microscopically  the  cortex  is  irregularly  thinned, 
and  the  arrangement  of  cell  layers  is  distorted.     The  third  and  next  the 


DISEASES    OF    THE   BRAIN 


411 


second  layers  are  the  most  affected.  The  nerve-cells  show  all  stages  of 
degeneration.  The  cortical  fibres  also  are  atrophied  and  in  the  last  stages 
of  the  disease  have  quite  disappeared,  the  supra-cortical  radial  fibres  being 
the  first  to  go.  The  neuroglia  tissue  is  greatly  increased  and  shows 
evidence  of  active  proliferation  and  finally  forms  sheaths  about  the  blood- 
vessels.    (Fig.  205.) 

The  blood-vessels  are  especially  affected.  There  is  an  active  for- 
mation of  new  vessels,  with  numerous  dilated  capillaries  and  widened 
adventitial  lymph  spaces.  These  spaces  are  filled  with  cells  which  are 
partly  lymphocytes   and  partly  plasma  cells.     This  vascular   change. 


Fig.  205. — Very  advanced  general  paresis.    A  vessel  of  the  gray  matter  showing  par- 
tially organized  periarteritis,  and  outside  of  this  a  neuroglial  sheath  ( X  320) .  (Bolton.) 

with  plasma  cells,  is  one  especially  characteristic  of  paresis  (Vogt,  Alzhei- 
mer). The  cells  are  large,  round  or  irregular  in  shape,  with  a  proto- 
plasmic body.  It  is  not  known  whether  they  come  from  connective 
tissue  or  the  leucocytes  of  the  blood. 

In  other  parts  of  the  brain  focal,  diffuse  and  tract  degenerations 
occur.  The  cerebellum  is  affected  like  the  cerebrum  but  to  a  less  degree. 
The  spinal  cord  shows  degenerations  in  both  the  posterior  and  lateral 
columns  in  about  two-thirds  of  the  cases.  Some  degenerative  changes 
occur  in  the  sympathetic  system  and  peripheral  nerves.  The  treponema 
pallida  has  been  found  deep  in  the  cerebral  tissues,  but  the  organisms 
are  few  in  number  and  difficult  to  detect.     The  explanation  of  how  they 


412 


DISEASES    OF   THE    NERVOUS   SYSTEM 


cause  such  an  extraordinary  disintegration  of  the  master  tissue  of  the  body- 
makes  a  long  chapter  in  pathology,  and  one  not  yet  completed. 

Prognosis. — The  prognosis  was  formerly  thought  to  be  invariably 
bad.  If  one  sees  the  patient,  however,  in  the  earliest  stage,  removes 
him  at  once  from  sources  of  excitement,  and  makes  him  live  quietly, 
using  anti-luetic  and  tonic  treatment,  one  can  sometimes  check  the  disease, 
and  practically  cure  it.  When  the  disease  has  well  entered  upon  its 
course  it  is  incurable  by  any  measures  as  yet  known. 

The  prognosis  is  better  the  more  the  symptoms  and  serological 
formula  suggest  meningeal  syphilis.  It  is  better  in  cases  in  which  the 
patient  shows  "insight"  as  to  his  condition;  better  when  the  mental 
symptoms  indicate  a  functional  psychosis  more  than  a  deterioration. 
Speech  defects  are  of  unfavorable  omen.  Tabo-paresis  has  about  the 
same  prognosis  as  paresis.  When  meningo-vascular  syphilis  exists,  if  a 
tabes  develops  paresis  does  not,  as  a  rule,  and  the  outlook  is  not  so  serious. 
Too  much  importance  may  be  placed  on  the  serological  formula.  It  may 
be  partly  positive  and  yet  the  patient  may  do  very  well.  Positive 
reactions  may  disappear  under  the  influence  of  time  and  good  hygienic 
conditions  alone. 

Laboratory  Tests  for  the  Presence  and  Differentiation  of  Syphilo- 
genous  Nervous  Disease. — The  serological  formulae  obtained  by  testing 
the  blood  serum  and  the  cerebrospinal  fluid  is  here  given  for  the  three 
important  luetic  nervous  diseases — meningo-vascular  syphilis,  tabes 
dorsalis,  paresis  and  tabo-paresis.  This  table  was  prepaied  by  Dr. 
David  Kaplan  of  the  N.  Y.  Neurological  Institute,  and  is  the  result  of 
over  two  thousand  complete  examinations.  Many  of  the  fluids  tested 
were  from  my  own  patients.  I  have  had  occasion  to  follow  this  work 
and  the  formulae  and  conclusions  given  agree  with  my  observations  up 
to  the  present  time. 


The  Serological 

Formulae 

Found  in  Syphilitic  Nervous  Diseases 

Cells 
per  oc. 

W.R.  in. 
C.S.F. 

Globulin. 

Fehl. 
Reduct. 

Colloid. 
Gold 

W.R.  in 
Serum 

I.  Meningo-vascul  a  r 

Average 

Plus 

Excess 

Present 

Present 

Plus 

Lues 

80  to  200 

in  65 

in  65 

in  95 

less  than 

in  80 

per  cent. 

per  cent. 

per  cent. 

2  per 
cent. 

per  cent. 

(Cerebral,  Spinal  or 

Extremes 

Cerebrospinal). 

0  to  2000 

II.   Tabes  Dorsalis 

Average 

Plus 

Excess 

Present 

Absent 

Plus 

35  to  60 

in  40 

in  33 

in  99 

in  65 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

Extremes 

0  to  350 

DISEASES    OF   THE   BRAIN 


413 


The  Serological  Foemul^  Found  in  Syphilitic  Nervous 
Diseases  . — Continued . 


Cells 
per  cc. 

W.R.  in 
C.S.F. 

Globulin. 

Fehl. 
Reduct. 

Colloid. 
Gold 

W.R.  in 
Serum 

III.  Paresis 

Average 

Plus 

Excess 

Present 

Present 

Plus 

18  to  35 

in  85 

in  75 

in  100 

in  95 

in  95 

and 

Extremes 
0  to  250* 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

Tabo-paresis 

20  to  40 

Plus 

Excess 

Present 

Present 

Plus 

in  85 

in  70 

in  100 

in  75 

in  95 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

per  cent. 

The  Wassermann  reaction  on  the  spinal  fluid  was  performed  by  using  0.5  cc.  of  the 
medium,  with  two  antigens;  one  containing  cholesterin. 

The  globulin  content  was  determined  by  the  butyric  acid  ammonium  sulphate 
method.  The  cells  were  counted  by  the  Fuchs-Rosenthal  method,  the  same  day  the 
fluid  was  obtained. 

Meningo-vascular  Lues. — This  form  represents  the  serology  of  the  earliest  in- 
volvement of  the  nervous  system.  The  increase  in  cells  may  appear  before  a  positive 
Wassermann  reaction  or  a  globulin  excess,  and  may  persist  until  cerebrospinal  func- 
tions are  impaired  and  detected  by  the  neurologist.  The  cell  count,  which  is  the  chief 
feature  of  this  pre-eminently  exudative  process,  may  reach  into  the  thousands,  but  is 
very  readily  influenced  by  treatment.  The  positive  fluid  Wassermann  reaction  dis- 
appears in  such  a  case  very  quickly,  and  if  a  great  many  cells  of  the  polynuclear 
variety  are  present,  thus  giving  rise  to  the  absent  Fehling  reduction,  the  latter  returns 
also  with  the  fall  in  the  pleocytosis  (increase  in  cells).  The  majority  of  cases  with  this 
form  of  luetic  nervous  involvement  show  on  an  average  from  80  to  180  cells  per  cubic 
millimetre  after  moderate  therapy.  In  this  form  of  lues  of  the  nervous  system  one  is 
able  to  do  away  entirely  with  abnormal  findings  in  less  time  and  with  fewer  remedies 
than  is  the  case  with  tabes  or  general  paresis.  Some  cases  remain  uninfluenced 
after  the  cell  count  reaches  20  to  30  per  cubic  millimetre,  using  the  intravenous  method 
of  salvarsanization.  In  case  the  intra-spinous  route  is  selected,  the  pleocytosis  is 
influenced  more  radically  on  a  mechanical  basis,  depending  chiefly  upon  the  removal 
of  the  cells  as  one  would  evacuate  an  abscess.  This  is  further  corroborated  by  the 
persistence  of  the  globulin  excess  and  the  positive  Wassermann  reaction  which  are 
to  be  regarded,  therefore,  as  an  expression  of  organic  response  not  depending  in  toto 
upon  the  local  disease. 

Tabes. — The  early  forms  of  this  disease  will  give  a  serology  closely 
resembHng  that  of  the  meningo-vascular  form  of  lues.  The  cell  count 
will  then  show  its  upper  limit,  the  globulin  will  give  an  intenser  precipita- 
tion than  in  the  later  stage,  and  the  Wassermann  reaction  will  be  positive 
in  both  media.  As  the  disease  progresses  and  assumes  its  more  or  less 
permanent  features,  the  serology  also  tends  to  settle  to  what  constitutes 
the  type  of  tabetic  serology.  The  Wassermann  reaction  in  the  serum 
is  positive,  that  of  the  fluid  is  negative,  or  only  weakly  positive,  the 
excess  of  globulin  is  less  marked   or  entirely   absent.     As   the   disease 


414  DISEASES    OF    THE    NERVOUS    SYSTEM 

progresses  and  enters  the  final  state,  the  entire  serology  may  become 
negative.  Unless  a  paretic  accompaniment  is  detected,  the  above 
holds  true  for  the  majority  of  tabetics.  If,  however,  paresis  becomes  an 
accompaniment,  the  serology  tends  to  assume  also  the  serological  features 
of  that  disease. 

Therapy  will  find  an  obstacle  in  some  cases  in  being  unable  to  render 
negative  a  positive  serum  Wassermann  (the  "Wassermann  fast"  phenome- 
non). The  Wassermann  reaction  in  the  fluid  will  also  manifest  itself 
together  with  a  comparatively  low  cell  count,  and  in  a  small  number 
of  cases  one  will  be  able  to  obtain  the  characteristic  curve  with  the  colloidal 
gold  as  found  in  general  paresis.  The  latter  form  is  entirely  different 
from  the  form  closest  to  the  meningo-vascular  type,  in  that  the  serology 
is  easily  rendered  negative,  and  the  high  cell  count  (hyperlymphocytic 
tabes)  will  be  found  to  fall  with  the  very  first  salvarsan  injection,  al- 
though given  intravenously.  The  fall  may  be  a  few  hundred  cells  to 
the  cubic  millimetre. 

General  Paresis. — Aside  from  furnishing  the  greatest  number  of 
cases  that  show  pathological  fluid  and  serum  changes,  this  disease  also 
furnishes  the  various  abnormal  constituents  in  its  greatest  intensity. 
The  ''Wassermann  fast  type"  is  a  feature  of  this  disease  more  often 
than  in  the  other  forms  of  lues  of  the  nervous  apparatus.  It  also  shows 
to  the  exclusion  of  the  other  forms  of  luetic  disorder,  the  characteristic 
precipitation  of  colloidal  gold,  which  is  one  of  the  most  constant  accom- 
paniments of  this  disease.  In  fact  where  one  is  able  in  rare  instances  even 
to  influence  the  W^assermann  reaction,  one  will  find  that  the  colloidal 
gold  phenomenon  still  persists.  In  early  paresis  one  will  occasionally 
find  an  absence  of  a  positive  Wassermann  reaction.  In  the  cerebro- 
spinal fluid,  the  pleocytosis  may  also  be  very  high,  comparatively, 
showing  thereby  the  common  origin  of  all  luetic  nervous  diseases,  which 
start  as  a  rule  with  a  high  cell  count  and  probably  with  a  meningo- 
vascular disturbance.  The  advanced  form  of  paresis  shows  the  full 
quota  of  abnormal  findings,  and  as  the  degenerative  process  advances,  one 
will  sometimes  miss  the  positive  Wassermann  reaction  in  the  serum, 
while  it  may  still  be  present  in  the  cerebrospinal  fluid.  In  the  latter 
instance  the  cell  count  may  be  very  near  the  normal  cell  count.  In 
some  cases  only  a  few  cells  were  encountered.  That  exceptions  may  be 
found  in  this  form  of  neural  lues  must  be  admitted,  so  that  one  will 
here  and  there  come  across  authentic  paresis  with  a  very  high  cell  count, 
amounting  to  200  or  300  cells  per  cubic  millimetre;  such  extreme  counts, 
however,  are  very  rare. 

Kaplan. 

Treatment. — The  first  and  most  important  thing  in  the  treatment  of 
paresis  in  its  early  stages  is  to  adopt  measures  for  the  treatment  of  syphilis 


DISEASES    OF    THE   BRAIN  415 

which  is  the  underlying  cause.  Before  the  advent  of  the  use  of  sal- 
varsan  this  was  done  by  the  intensive  use  of  mercury  and  iodides 
combined  with  ehminative  measures,  tonics  and  fresh  air.  These  measures 
were  not  without  distinct  success  and  it  even  remains  still  to  be  proved 
that  salvarsan  treatment  is  more  permanently  efficacious  than  the 
older  methods. 

There  has  been  of  late  years  so  much  more  interest  and  effort  in 
the  treatment  of  paresis  that  enormously  better  results  are  being  obtained, 
apparently,  by  the  new  method,  but  certainly  to  some  extent  by  reason 
of  greater  interest  now  taken  in  therapeutics. 

The  technical  methods  of  using  salvarsan  and  its  preparations  differ 
with  different  practitioners,  and  the  final  and  best  methods  have  not 
yet  been  agreed  upon.  The  technic  which  the  writer  employs  and 
which  has  been  used  to  a  large  extent  in  the  New  York  Neurological 
Hospital,  is  as  follows: 

The  patient  is  given  an  intravenous  injection  of  0.45  neo-salvarsan. 
After  an  interval  of  two  days  he  is  given  another  injection  of  0.9  and  this 
injection  is  repeated  every  third  day  until  he  has  had  ten  injections. 

During  the  time  that  these  injections  are  given  he  receives  either  a 
hypodermic  of  one  grain  of  salicylate  of  mercury  twice  a  week,  or  daily 
inunctions  of  mercury  on  the  days  on  which  he  does  not  receive  the  intra- 
venous injection. 

After  the  patient  has  received  the  tenth  dose,  he  is  given  a  prescrip- 
tion containing  gr.  ^^^4  of  bichloride  of  mercury  and  gr.  x.  of  iodide  of 
potassium  and  this  he  takes  intermittently  for  the  following  four  weeks. 

After  this  he  is  given  an  intra-venous  injection  of  neo-salvarsan  every 
month  for  five  months  and  then  is  given  another  intensive  treatment, 
if  the  remission  or  improvement  is  not  completely  satisfactory. 

The  intra-venous  injections  are  continued  for  a  period  of  a  year  but 
with  less  frequency.  They  should  be  continued  intensively  irrespective 
of  the  condition  of  the  blood  and  cerebrospinal  fluids.  The  endeavor 
to  measure  the  amount  of  treatment  which  should  be  given  by  the 
laboratory  findings  of  these  fluids  is  a  mistake,  or  at  least  these  things 
should  not  be  too  closely  followed  as  therapeutic  guides. 

Naturally,  while  carrying  out  this  technic,  a  proper  regard  should 
be  had  for  the  general  condition  of  the  patient's  health,  and  measures 
such  as  laxatives,  tonics,  fresh  air  and  rest  should  all  be  instituted. 

The  method  thus  outlined  as  a  standard  one  needs  variations  in  ac- 
cordance with  the  state  of  the  disease  and  its  rate  of  progress.  When 
there  is  evidence  of  an  associated  meningeal  exudate  the  number  of 
injections  may  be  increased  and  even  brought  more  closely  together. 
I  have  seen  a  very  good  result  from  giving  0.9  neo-salvarsan  daily  for  nine 
days.     It  seems  that  the  nearer  one  can  come  to  safe  toxic  doses  the 


416  DISEASES    OP   THE    NERVOUS    SYSTEM 

better  results  will  be  achieved  and  for  this  reason  it  may  be  wise  to  give 
an  intra-spinous  injection  of  salvarsanized  serum,  or  salvarsanized 
serum  with  the  addition  of  neo-salvarsan  itself  in  connection  with  this 
and  in  addition  to  the  regular  intra-venous  injections.  It  may  be  neces- 
sary to  give  as  many  as  thirty  injections  in  the  course  of  two  or  three 
months. 

There  is  still  a  difference  of  opinion  as  to  the  relative  value  of  salvarsan 
and  neo-salvarsan,  it  being  generally  believed  that  the  salvarsan  is 
about  twice  as  powerful  as  the  neo-salvarsan,  but  that  it  does  not  act 
more  beneficially,  except  for  the  fact  that  it  is  stronger. 

The  earlier  in  the  course  of  the  disease  that  treatment  is  given  the 
better  the  outlook.  On  the  other  hand,  in  the  third  and  terminal  stage 
of  the  disease  the  treatment  is  useless  and  may  even  hasten  the  death  of 
the  patient.  It  seems  wise  in  some  more  chronic  cases  to  give  a  series 
of  injections  of  mercury  before  giving  salvarsan. 

Opinions  also  still  differ  as  to  the  value  of  the  intra-spinous  injections 
of  salvarsanized  serum  (Swift-Ellis  method)  and  of  the  intra-spinous 
injections  of  the  patient's  serum  to  which  salvarsan  is  added.  I  have 
not  seen  any  convincing  evidence  that  the  method  is  a  superior  one, 
but  there  are  some  who  very  strongly  support  it. 

In  the  use  of  this  method  injections  are  given  not  oftener  than  once 
in  ten  days  or  two  weeks,  and  the  number  of  injections  is  generally 
determined  by  the  effect  of  them  upon  the  cerebrospinal  fluid  reactions. 
It  has  been  found  comparatively  easy  to  reduce  the  number  of  cells  to 
the  normal  amount  in  the  cerebrospinal  fluid  by  the  various  methods  of 
treatment,  but  to  make  the  blood  and  cerebrospinal  fluid  negative  to 
the  Wassermann  reaction  in  true  paresis  is  very  difficult. 

The  result  of  treatment  in  early  cases  is  almost  invariably  to  secure 
a  satisfactory  remission,  and  these  remissions  in  many  cases  are 
practically  like  cures. 

The  doctrine  put  forth  by  certain  neurologists  that  when  parenchy- 
matous degeneration  of  the  brain  sets  in,  treatment  is  useless,  is  certainly 
untrue  and  not  founded  on  any  sound  pathological  basis.  We  know  per- 
fectly well  that  parenchymatous  degeneration  of  locomotor  ataxia  is 
often  arrested  and  patients  live  for  thirty  years  or  more.  We  also  know 
that  remissions  have  occurred  in  paresis  lasting  many  years. 

Aside  from  the  treatment  thus  outlined  the  therapeutics  of  paresis 
is  mainly  tonic  and  symptomatic,  in  the  second  and  third  stages. 

Various  other  specific  treatments  of  paresis  have  been  suggested  and 
tried,  such  as  the  injections  of  nucleinate  of  soda  and  of  tuberculin  to 
produce  artificial  fever.  I  have  not  seen  any  successes  from  these  forms  of 
treatment. 


DISEASES    OF    THE   BRAIN  417 

Naturally  the  patient  while  undergoing  specific  treatment  should  be 
under  close  observation  and  be  made  to  live  a  quiet  and  regular  life. 
The  influence  of  a  life  entirely  in  the  open  air  is  of  great  value  in  ameliorat- 
ing the  luetic  infection.  I  have  seen  the  serological  formula  become 
negative  just  by  this  means. 

MULTIPLE  SCLEROSIS 

Multiple  sclerosis  is  a  chronic  and  intermittently  progressive  malady 
characterized  by  some  paralysis,  usualty  in  the  form  of  paraplegia,  by 
coarse  tremor,  disturbances  of  speech,  nystagmus,  apoplectiform 
attacks,  and  various  other  cerebral  and  spinal  symptoms  depending 
upon  the  seat  of  the  lesion.  It  is  due  to  the  development  of  sclerotic 
patches  in  the  different  parts  of  the  brain  and  cord,  which  patches 
are  for  the  most  part  the  result  of  a  neuroglia  proliferation.  The  disease 
is  probably  an  inflammatory  rather  than  a  degenerative  one.  It  affects 
the  spinal  cord  as  well  as  the  brain. 

Etiology. — It  occurs  rather  more  frequently  in  the  male  sex  and 
is  a  disease  of  the  first  half  of  life.  Multiple  sclerosis  is,  in  fact,  one  of 
the  few  chronic  nervous  disorders  of  organic  origin  developing  at  this 
time.  Most  cases  begin  between  the  age  of  twenty  and  thirty.  Cases 
have,  however,  been  observed  in  infants  and  children,  but  the  trouble 
in  its  typical  forms  does  not  appear  in  the  declining  years  of  Kfe.  While 
a  few  cases  of  hereditary  multiple  sclerosis  have  been  reported,  it  is 
generally  conceded  that  hereditary  influence  is  very  slight  and  even  a 
hereditary  tendency  to  degenerative  disease  or  a  neuropathic  family 
history  is  rare  though  not  unknown.  Strumpell's  theory  that  the 
disease  is  endogenous  has  not  been  sustained.  There  can  be  no  doubt 
that  the  most  important  of  all  of  the  few  known  causes  of  multiple 
sclerosis  is  infection.  This  is  so  true  that  it  may  be  called  a  post-infec- 
tious disease.  The  infectious  disorders  which  are  followed  by  sclerosis 
are  typhoid  fever,  pneumonia,  malaria,  and  the  eruptive  fevers.  It  has 
been  known  to  follow  also  diphtheria,  whooping-cough,  erysipelas,  dys- 
entery, cholera,  and  even  rheumatism.  Another  important  cause  is 
excessive  muscular  exertion,  such  as  occurs  in  professional  dancers, 
and  amateur  or  professional  athletes.  Workers  in  metallic  poisons, 
such  as  lead,  copper,  zinc,  and  even  manganese  may  develop  sclerosis. 
The  influence  of  trauma  in  causing  multiple  sclerosis  has  to  be  very 
carefully  weighed.  It  is  certainly  very  rare,  but  there  seem  to  be  some 
few  cases  in  which  trauma  appeared  to  be  an  exciting  cause.  It  is 
generally  accepted  that  neither  syphilis  nor  alcoholism  are  causative 
factors,  although  syphilis  may  be  associated  with  the  disease  and  perhaps 
produce  a  peculiar  luetic  form  of  it. 

27 


418  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  following  data  as  to  the  frequency  and  cause  of  the  disease 
were  collected  by  Dr.  C.  W.  0.  Bunker,  in  his  neurological  prize  essay: 

Frequency. — Among  70,000  neurological  cases  in  America  the  percentage  of 
multiple  sclerosis  was  1  in  266,  or  0.058  per  cent.  In  Scotland  it  is  about  2  per  cent.; 
in  Berlin,  0.85  per  cent.;  in  Hamburg,  1  per  cent. 

Age. — The  following  table,  compiled  by  Bunker  and  myself,  represents  American 
cases.  It  makes  the  incidence  of  the  disease  too  late.  Practically,  the  cases  occur 
between  the  fifteenth  and  thirty-fifth  years. 

-10,  9 
10-20,  17 
20-30,  36 
30-40,  45 
40-50,  32 
50-60,  24 
60-70,  7 
70-80,    4 

The  disease  is  twice  as  frequent  in  men  as  women — 129  to  67;  statistics  of  Jelliffe, 
Bunker  and  myself.  European  statistics  make  the  numbers  about  even.  The  dis- 
ease is  seen  more  frequently  in  foreigners,  perhaps,  because  our  clinics  are  so  largely 
foreign  in  population.     My  private  cases  are  nearly  all  American. 

Symptoms.- — The  disease  begins  insidiously.  There  may  be  a  pre- 
liminary and  rather  short  hemiplegic  or  paraplegic  attack  with  some 
sensory  disturbance.  More  often  a  comparatively  short  time  after 
recovery  from  some  acute  disease  the  patient  begins  to  suffer  from 
weakness  of  the  lower  limbs  with  stiffness  and  some  degree  of  heaviness, 
and  numbness.  The  bladder  is  also  a  little  weak,  and  it  is  difficult  to 
retain  the  urine.  These  symptoms  after  a  few  weeks  may  disappear 
and  the  patient  be  well  for  months.  If  not,  very  soon  the  patient 
notices  some  unsteadiness  in  the  gait,  due  not  alone  to  weakness  in 
the  legs,  but  to  an  increasing  degree  of  ataxia.  He  finds  also  that  his 
hands  are  trembling  and  that  this  tremor  increases  upon  voluntary  motion. 
It  is  the  type  of  tremor  known  as  ''intentional."  He  has  at  this  time 
also  some  indistinctness  in  speech,  it  being  difficult  for  him  to  enunciate 
long  words.  These  come  out  in  a  slow,  syllabic  utterance,  as  it  is  called, 
each  syllable  being  spoken  separately.  He  may  have  also  a  little  trouble 
in  swallowing.  By  this  time  he  has  had  some  sensation  of  numbness  in 
the  limbs,  and  some  pains  occasionally  in  the  joints  and  extremities,  but 
the  sensory  troubles  are  not  permanent  or  not  very  marked  and  are 
mainly  parsesthesic.  If  he  is  examined  now  it  will  be  found  that  the  gait 
is  stiff  and  awkward,  the  patient  walking  unsteadily;  or,  in  other  cases,  it 
may  simply  be  the  stiff,  weak  gait  of  moderate  paraplegia.  The  Romberg 
symptom  will  be  found  to  be  present  to  some  extent.  The  knee-jerks 
are  exaggerated  and  ankle  clonus  and  Babinski's  reflex  may  be  present. 
The  abdominal  reflexes  are  absent  early  in  many  cases.     Ihe  hands  are 


DISEASES    OF    THE   BRAIN 


419 


unsteady,  and  the  movements  are  characterized  by  a  jerky  tremor, 
which  may  be  so  great  that  the  patient  has  difficulty  in  dressing  and  feed- 
ing himself.  This  tremor  disappears  almost  entirely  if  the  patient  lies 
flat  upon  his  back.  If  he  sits  up,  however,  it  may  be  seen  perhaps  in  the 
muscles  of  the  neck,  causing  the  head  to  be  oscillated,  and  constantly 
more  or  less  regular  tremor  in  the  arms  is  present.  As  the  disease  pro- 
gresses the  speech  becomes  more  thick,  and  often  is  almost  unintelligible 
in  the  severer  cases.  Examination  of  the  eyes  shows  a  nystagmus,  per- 
haps only  when  the  eyes  are  turned  to  one  side,  but  often  the  jerky 
movements  are  seen,  even  when  the  patient  is  told  to  look  directly  at 


Fig.  206. — Pallor  of  entire  optic  disc  except  its  nasal  margin.     {Holden.) 

an  object.  Evidence  of  impaired  eyesight  appears  with  pallor  of  the 
temporal  side  of  the  optic  disc  (Fig.  206),  and  a  central  scotoma  may 
be  noted.  The  tongue  is  protruded  in  a  jerky  way,  and  attempts  at 
swallowing  are  often  awkward.  If  a  glass  of  water  is  handed  him, 
the  patient  seizes  it,  but  in  carrying  it  to  his  mouth  he  agitates  it  so 
violently  that  the  fluid  is  spilled  and  perhaps  the  tumbler  drops  from 
his  hands.  Examination  of  the  muscular  system  shows  weakness  of  the 
legs,  less  of  the  arms,  but  no  complete  paralysis.  There  is  no  marked 
atrophy  of  the  limbs,  and  no  change  of  any  moment  in  the  electrical 
reactions.     There  are  many  cases  in  which  the  jerky  tremor,  syllabic 


420  DISEASES    OF    THE    NERVOUS    SYSTEM 

speech  and  nystagmus  are  not  marked  or  develop  very  slowly,  and  more 
recent  studies  show  that  the  most  common  symptoms  are: 

1.  Bladder  weakness. 

2.  Absence  of  abdominal  reflexes. 

3.  Spastic  paraplegia. 

4.  Optic  atrophy. 

5.  Sensory  defect  (parsesthesise) . 

6.  Sphincter  trouble. 

7.  Speech  defect. 

Examintion  of  the  cutaneous  sense  may  show  some  little  tactile 
anaesthesia  in  the  limbs,  but  this  is  not  always  present  and  in  general 
the  cutaneous  sensory  disturbances  are  slight  and  evanescent.  There  is 
a  certain  amount  of  ataxia,  which  is  not  due  to  muscular  anaesthesia  but 
to  inability  to  control  and  co-ordinate  the  movements.  There  is  no 
loss  of  sense  of  weight  or  of  pressure.  Of  the  nerves  of  special  sense, 
the  eye  is  most  frequently  involved.  The  patient  may  have  some  diplopia 
from  paralysis  of  one  of  the  eye-muscles.  The  pupils  react  to  light  and 
accommodation.  The  involvement  of  the  optic  nerve  may  go  on  to 
an  almost  complete  atrophy.  On  account  of  this  the  patient  suffers 
from  contraction  of  the  visual  field,  central  and  other  scotomata,  and 
weakness  of  vision,  but  absolute  blindness  never  occurs.  Examination 
of  the  cerebrospinal  fluid  by  lumbar,  puncture  shows  the  absence  of  a 
lymphocytosis. 

While  the  disease  is  running  the  course  just  described,  the  patient 
sometimes  suffers  from  attacks  of  vertigo,  and  occasionally  from  sudden 
seizures  resembling  apoplexy,  and  even  from  epileptiform  attacks. 
The  mind  is  usually  not  much  affected,  and  I  do  not  recognize  any  special 
mental  characteristics  except  a  certain  childishness  of  temperament. 
There  may,  however,  be  some  slight  dullness  of  the  intellect,  some  hebe- 
tude, or  even  a  slight  amount  of  melancholia.  In  certain  cases  the 
patients  are  subject  to  attacks  of  impulsive  laughing;  that  is  to  say, 
without  any  sufficient  cause  they  suddenly  break  out  in  exaggerated 
laughter,  from  which  they  quickly  recover  themselves.  These  attacks 
are  due  the  cerebral  lesions.  As  the  patient  gets  worse  the  paraplegia 
increases  and  he  becomes  finally  helpless.  The  use  of  the  arms  is  pre- 
served for  a  longer  time.  Involvement  of  the  sphincter  of  the  bladder 
occurs  early,  that  of  the  rectum  very  late  if  at  all. 

The  progress  of  the  affection  is  variable.  It  usually  progresses  slowly 
with  some  remissions,  reaching  finally  in  two  or  three  years  a  chronic 
stage,  in  which  the  patient  remains  for  several  years  without  much  change. 
At  other  times  the  progress  of  the  disease  is  hastened  by  repeated  ex- 
acerbations,    accompanied    by    apoplectiform    or    hemiplegic    attacks. 


DISEASES    OF    THE   BRAIN 


421 


In  still  other  cases  the  amelioration  continues  and  remains  permanent, 
and  a  practical  cm'e  takes  place. 

Types. — The  various  symptom  groups  of  the  disease  are  classified  as 
cerebro-cerebellar,  and  spinal.  The  cerebro-cerebellar  symptoms  con- 
sist in  modifications  of  speech,  attacks  of  vertigo  and  apoplectiform 
seizures,  hemiplegia,  intention  tremor,  labyrinthine  symptoms,  mental 
changes,  optic  atrophy  and  spasmodic  laughing  or  crying.  There  is 
sometimes  also  a  certain  amount  of  deafness  and  perversion  of  taste  and 
smell. 

In  the  not  uncommon  spinal  type,  the  dominant  symptoms  are  the 
spasmodic  paraplegia,  with  some  bladder  and  sexual  weakness,  and  a 
slight  amount  of  sensory  trouble.  There  may  be  also  some  weakness 
and  unsteadiness  of  the  arms,  but  the  cranial  nerves  are  not  involved. 


Fig.  207.- 


-Multiple  sclerosis,  showing  lesions  of  the  cord. 
Dr.  Charles  I.  Lambert.) 


{From  photograph  by 


Aborted  Types. — In  some  cases  the  nodules  of  sclerosis  are  so  limited 
in  number  and  so  peculiarly  placed  that  they  give  rise  to  very  atypical 
and  mild  forms  of  the  disease. 

Pathology. — Grayish  nodules  are  found  distributed  through  the 
brain  and  spinal  cord  (Figs.  207-208),  They  vary  in  size  from  a  milli- 
metre to  two  or  three  centimetres  in  diameter  (one  twenty-fifth  to  one 
inch).  They  are  of  firmer  consistence  than  is  the  surrounding  brain 
substance,  but  are  not  quite  so  hard  as  is  ordinary  connective  tissue. 
They  consist  microscopically  of  neurogha  tissue,  which  some  assert  to 
be  connected  with  the  walls  of  the  blood-vessels,  as  a  rule.  Very  often 
the  axis-cyhnders  of  nerves  can  be  seen  passing  through  the  lesion.  The 
nodules  are  found  most  frequently  in  the  white  matter  of  the  brain,  more 
especially  in^the  pons,  internal  capsule,  and  centrum  ovale.     They  rarely 


422 


DISEASES    OF    THE    NERVOUS    SYSTEM 


begin  primarily  in  the  gray  matter,  but  may  invade  it  secondarily. 
The  roots  of  the  peripheral,  especially  of  the  cranial,  nerves  occasionally 
contain  or  are  surrounded  by  these  sclerotic  masses.  In  the  spinal 
cord  they  may  extend  up  and  down  the  gray  and  white  matter  for  a 
considerable  distance,  or  they  may  involve  the  whole  cord  at  a  certain 
level,  turning  it  into  a  fibrous  mass.  The  blood-vessels  surrounding  and 
in  connection  with  these  diseased  areas  show  some  evidences  of  thickening 
and  increased  vascularity,  but  no  true  inflammatory  process,  as  a  rule. 
The  primary  pathological  change  in  multiple  sclerosis  is  as  yet  unknown; 
many  things  point  to  its  starting  originally  from  small  emboli  or  thrombi 
which  lead  to  minute  softenings,  with  a  secondary  reparative  and  sclerotic 


Fig.  208. — Multiple  cerebrospinal  sclerosis.     {Charcot.) 


process.  The  fact  that  the  disease  follows  infective  fevers  makes  such 
an  origin  of  it  seem  probable.  On  the  other  hand,  pathological  anatomy 
does  not  yet  bear  out  this  view,  and  it  is  possible  that  the  disease  begins 
by  a  primary  degeneration  affecting  first  the  myelin  sheaths  of  the 
nerve-fibres  sparing  the  axis-cylinders  and  cell  bodies,  this  being  followed 
by  a  neurogha  and  connective-tissue  proliferation  which  ends  in  the 
formation  of  the  small  islands  of  sclerosis.  An  important  pathological 
peculiarity  of  the  process  is  that,  while  it  destroys  the  myelin  sheaths 
of  the  nerves,  the  axis-cylinders  remain  intact  for  a  long  time,  and  con- 


DISEASES    OF    THE   BRAIN  423 

sequentlj^  conduction  of  nerve  impulses  takes  place  imperfectly,  directly 
through  the  nodular  masses. 

Course  and  Duration. — The  disease  runs  a  very  irregular  course 
Its  prodromal  stage  is  long  and  remissions  of  considerable  length  occur. 
The  disease  may  last  from  ten  to  thirty  years,  the  average  duration 
being  five  to  ten  years.  Death  sometimes  occurs  from  involvement  of 
the  nerves  of  the  medulla,  but  more  often  from  weakness  and  exhaustion 
or  some  intercurrent  malady. 

Diagnosis. — The  diagnosis  in  typical  cases  is  not  very  difficult;  but 
as,  on  the  other  hand,  typical  cases  are  not  common,  the  disease  has 
always  to  be  studied  with  great  care  before  certainty  can  be  reached. 
The  diagnosis  is  based  upon  the  slow  development  of  the  disease,  with 
attacks  of  vertigo,  weakness,  parsesthesia  and  uncertainty  in  gait;  also 
upon  the  paralysis  of  the  extremities,  the  intention  tremor,  ataxia, 
rigidity  and  contractures;  upon  the  disturbances  of  vision,  nystagmus; 
loss  of  abdominal  reflexes,  and  the  speech  troubles.  The  existence  of 
early  paralysis  with  parsesthesise,  or  of  parsesthesise  alone  followed  by 
remission,  is  most  significant.  The  presence  of  headaches,  attacks  of 
vertigo,  apoplectiform  attacks,  and  the  pecuhar  mental  condition  often 
furnish  help.  The  age  of  the  patient  and  the  cause  should  also  be  taken 
into  consideration.  The  disease  must  be  distinguished  from  Friedreich's 
ataxia,  spastic  spinal  paralysis,  locomotor  ataxia,  dementia  paralytica, 
bulbar  paralysis,  paralysis  agitans,  chronic  meningitis,  and  hysteria. 
The  points  already  given  and  those  furnished  under  the  heads  of  these 
different  diseases  must  be  utihzed  in  making  these  distinctions.  In 
the  pseudo-sclerosis  of  Westphal,  there  are  no  ocular  symptoms.  In 
diffuse  cerebral  sclerosis,  also,  ocular  symptoms  are  rare  and  there 
are  progressive  dementia  and  paralysis.  In  multiple  sclerosis  the  pupils 
are  rarely  affected.  The  method  of  exclusion  may  be  used  with  advantage 
in  reaching  the  diagnosis  of  this  protean  malady. 

Prognosis. — The  prognosis,  whUe  not  favorable  as  regards  the  ulti- 
mate cure,  is  somewhat  favorable  as  regards  a  remission  and  improve- 
ment, and  the  disease  on  the  whole  is  not  so  severe  as  is  locomotor  ataxia 
or  the  other  degenerative  disorders. 

A  quiet  regular  life  is  very  necessary,  and  at  certain  intervals  the 
patient  should  go  to  bed  for  several  days.  Systematic  re-educational  exer- 
cises are  to  be  used  for  very  short  periods.  Electricity  is  of  Uttle  value 
except  for  symptoms.  Hypodermic  injections  of  the  cacodylates;  also 
those  of  salvarsan  and  of  fibrolysin  are  useful.  Urotropin  may  be  given 
for  short  periods  in  large  doses.  Occasional  courses  of  iodides  and  mer- 
cury are  beneficial.     Atropin  and  belladonna  are  useful  symptomatically. 

If  the  case  is  taken  early  and  the  patient  works  for  his  cure  hopefully 
and  earnestly  much  may  be  accomplished. 


424  DISEASES    OF    THE    NERVOUS    SYSTEM 

THE  APOPLEXIES 

Apoplexy  is  a  clinical  term  used  to  indicate  a  condition  characterized 
by  sudden  paralysis,  usually  attended  with  loss  of  consciousness,  and  due 
to  the  breaking  or  blocking  up  of  a  blood-vessel  in  the  brain. 

Apoplexy  is  a  general  term.  Particular  forms  are  described  in  ac- 
cordance with  the  cause  of  the  apoplexy.     These  are: 

1.  Intracranial  hemorrhage,  from  rupture  of  a  blood-vessel  (hemor- 
rhagic apoplexy). 

2.  Acute  cerebral  softening,  from  embolism  or  thrombosis  (embolic 
or  thrombotic  apoplexy). 

APOPLEXY  FROM  INTRA-CRANIAL  HEMORRHAGE 

(Cerebral  Hemorrhage,  Hemiplegia) 

There  are  four  groups  of  intra-cranial  blood-vessels :  those  of  the  dura 
mater,  those  of  the  pia  mater,  those  supplying  the  basal  ganglia  and 
white  matter,  and  those  supplying  the  pons,  medulla,  and  cerebellum. 
These  last  are  chiefly  branches  of  the  vertebrals  and  are  a  separate 
group,  subject  to  somewhat  different  mechanical  conditions.  Corre- 
sponding to  this  we  have: 

1.  Dural  or  pachymeningeal  hemorrhages. 

2.  Pial  or  subarachnoid  hemorrhages. 

3.  Central  or  capsular  hemorrhages. 

4.  Hemorrhages  in  the  medulla,  pons  and  cerebellum. 

It  is  the  central  hemorrhages  (No.  3),  due  to  rupture  of  the  blood- 
vessels going  to  the  great  basal  ganglia,  internal  capsule,  and  white 
matter,  that  constitute  the  great  majority  of  cerebral  hemorrhages 
seen  by  the  physician.  It  is  this  class  that  I  have  particularly  in  mind 
in  the  following  description. 

Etiology. — -At  the  time  of  birth  and  during  infancy  there  is  a  slight 
tendency  to  intra-cranial  hemorrhage  owing  to  the  accidents  and  injuries 
of  labor.  The  hemorrhages  at  birth  are  usually  meningeal  and  traumatic. 
After  this  period  the  liability  is  very  small,  but  slowly  increases  up  to 
the  age  of  forty,  when  predisposition  specially  begins.  Four-fifths  of 
all  cases  occur  after  forty,  and  the  tendency  to  hemorrhages  increases 
in  each  decade  up  to  eighty,  when  it  diminishes  absolutely  and  relatively. 
Males  are  slightly  more  predisposed  than  females.  Rather  more  cases 
occur  in  cold  weather,  at  high  altitudes,  in  the  temperate  zone,  and 
among  civilized  races.  With  the  improvement  in  general  health  condi- 
tions and  the  greater  average  longevity,  there  is  an  increase  in  apoplexies. 
Hereditary  tendencies  are  most  important.  This  tendency  is  to  arterial 
degeneration  and  often  runs  in  families.     Excessive  eating  and  drinking. 


DISEASES    OF    THE   BRAIN  425 

excessive  work,  and  anxiety  of  mind,  in  fine  all  the  causes  leading  to 
arterial  disease,  predispose  to  cerebral  hemorrhage.  Syphilis  is  more 
often  a  cause  of  thrombosis.  It  was  present  in  over  20  per  cent,  of  my 
cases  of  cerebral  hemorrhage,  while  kidney  disease  was  present  in  one- 
third  of  the  cases. 

Congenital  anomalies,  such  as  a  narrow  thoracic  aorta  or  inherited 
deficiency  in  the  strength  of  the  walls  of  the  blood-vessels,  also  play  a 
part.  Any  sudden  physical  exertion,  such  as  straining  at  stool,  the  ex- 
citement at  coitus  or  of  a  passion,  eating  a  large  meal  and  drinking 
a  great  deal  of  fluid,  especially  alcohol,  taking  a  cold  bath,  all  ma}^  lead  to 
rupture  of  an  artery.  Direct  blows  on  the  head  may  cause  meningeal 
hemorrhage,  rarely  a  central  hemorrhage,  for  the  central  blood-vessels 
are  well  protected.^ 

The  symptoms  are  the  prodromal,  those  of  the  attack  and  acute  stage, 
and  those  of  the  chronic  stage. 

Prodromal  symptoms  are  rare  except  in  syphilitic  cases.  When 
present  the  patient  suffers  from  headache,  insomnia,  dizziness,  numb- 
ness of  the  hand  and  foot  on  one  side,  and  a  failure  of  memory  for  words. 
He  may  have  "full"  feelings  or  even  pain  in  the  head  and  bad  dreams 
at  night.  Nosebleed  and  irregular  heart  action  sometimes  occur. 
Often  attack  comes  on  when  the  patient  is  feeling  particularly  well. 
The  attack  always  comes  on  suddenly  and  may  be  accompanied  (1)  by 
convulsions  and  coma,  (2)  by  coma  alone,  or  (3)  it  may  come  without  loss 
of  consciousness. 

1.  Initial  convulsions  are  rare  and  generally  mean  a  meningeal 
hemorrhage.  They  occur,  however,  in  young  children.  When  present 
they  are  unilateral  or  partial,  as  a  rule,  but  may  be  general.  2.  The 
common  mode  of  onset  is  with  coma.  The  patient,  without  warning, 
suddenly  becomes  dizzy,  loses  consciousness,  and  falls.  The  face  is 
flushed,  the  pulse  hard  and  rather  slow,  the  blood-pressure  may  rise 
to  over  200  mm.,  the  breathing  is  labored  and  stertorous,  the  cheek  on 
one  side  puffs  out  with  each  expiration,  the  eyes  are  partly  closed,  the 
eye-balls  fixed  or  deviated  to  the  paralyzed  side,  the  pupils  are  contracted 
and  rigid,  the  skin  is  bathed  in  sweat,  the  limbs  are  relaxed,  but  some 
evidence  of  hemiplegia  is  present  and  the  Babinski  reflex  can  be  usually 
elicited;  the  urine  may  be  retained  or  it  and  the  feces  involuntarily  evacu- 
ated. The  urine  is  usually  of  rather  high  specific  gravity  and  often  con- 
tains albumin,  even  when  there  is  no  renal  disease.  The  temperature 
in  severe  cases  may  fall  below  normal  during  the  first  twelve  hours,  even 
to  96°  F.,  but  this  is  not  the  rule.     It  is  the  rule,  however,  for  the  tem- 

1  Among  324  cases  of  hemiplegia  occurring  in  the  Cornell  clinic,  carefully  analyzed 
by  Dr.  T.  W.  Evans,  he  found  less  than  1  per  cent,  in  which  even  the  question  of 
trauma  could  be  raised.  Among  120  private  cases,  there  was  a  history  of  a  blow  and 
of  syphilis  in  one. 


426 


DISEASES    OF   THE    NERVOUS    SYSTEM 


perature  in  a  few  hours  to  be  K°  or  1°  higher  on  the  paralyzed  than  on 
the  sound  side.  If  the  case  is  rapidly  fatal,  coma  continues,  respiration 
often  assumes  a  Cheyne-Stokes  character,  the  pulse  becomes  fast,  the 
blood  tension  falls  and  symptoms  of  bulbar  failure  occur;  the  temperature 
gradually  rises,  and  usually  reaches  102°  or  103°  F.,  until  just  before 
death,  when  it  may  sink  again.     Swallowing  and  speech  become  difficult, 

hypostatic  pneumonia  sets  in,  and 
the  patient  dies  in  from  two  to  four 
days.  In  slower  fatal  cases  the  pa- 
tient regains  consciousness  partially 
and  then  enters  a  condition  of  stupor 
or  mild  delirium.  He  is  restless  and 
suffers  from  headache.  The  tempera- 
ture may  continue  normal  for  a  time, 
but  is  usually  higher  on  the  affected 
side.  At  the  end  of  two  or  three 
weeks  it  rises  higher,  pneumonia  may 
develop,  the  patient  becomes  uncon- 
scious, and  death  ensues.  In  the 
favorable  cases,  which  constitute  the 
majority,  coma,  if  present,  gradually 
passes  away  in  from  one  to  six  hours, 
leaving  the  patient's  mind  somewhat 
weak  and  confused  and  his  speech 
disturbed,  or  more  rarely  the  intelU- 
gence  may  not  be  at  all  disturbed. 
During  the  first  few  days  or  weeks 
after  the  attack  the  physician  finds 
that  the  prominent  symptom  is  the 
hemiplegia.  This  affects  the  arm  and 
leg  most  and  the  face  least.  Only 
the  lower  two  branches  of  the  facial 
nerve  are  involved,  and  the  patient 
can  shut  the  eyes.  The  tongue,  if 
protruded,  turns  to  the  paralyzed 
side;  the  uvula  is  turned  in  various 
ways  and  its  position  is  of  no  significance.  There  is  often  some  evidence 
of  cutaneous  anaesthesia  of  the  paralyzed  side,  and  less  often  hemi- 
anopsia and  disturbances  of  hearing  occur.  In  right-sided  hemiplegia 
the  patient,  after  recovering  consciousness,  is  often  unable  to  talk  or 
to  understand  what  is  said.  Examination  shows  that  he  has  a  motor 
or  sensory  aphasia  (vide  Aphasia). 


Fig.  209. — Chronic  hemiplegia  with 
contractures.      {Curschniann.) 


DISEASES    OF    THE   BRAIN  427 

The  deviation  of  the  eyes  and  head  to  one  side  usually  disappears 
in  a  day  or  two.  Occasionally  there  is  a  temporary  ptosis.  The  pupils 
at  j&rst  are  contracted,  that  on  the  paralyzed  side  the  more  so;  this  con- 
dition disappears  with  returning  consciousness. 

The  paralysis  of  the  arm  and  leg  is  usually  flaccid  at  first,  and  the 
hmb  falls  heavily  when  hfted;  the  reflexes  are  lessened  or  abohshed. 
In  a  few  days  rigidity  and  exaggeration  of  the  deep  reflexes  appear  on  the 
paralyzed  side,  with  ankle  clonus  and  dorsal  flexion  of  the  big  toe. 

Sometimes,  however,  rigidity  sets  in  at  once.  This  symptom  occurs 
when  the  blood  has  broken  into  the  ventricles,  and  also  in  some  menin- 
geal hemorrhages.  The  skin  reflexes,  particularly  the  abdominals  are 
lost  on  the  paralyzed  side. 

The  usual  course  of  the  temperature  is  for  it  to  rise  on  the  second 
and  third  day  to  100°F.  or  102°F.,  being  1^°  to  1°  higher  on  the  paralyzed 
side.  In  a  few  days  it  gradually  falls,  so  that  by  the  eighth  to  the  tenth 
day  it  is  normal. 

If  the  temperature  continues  to  rise  after  the  fourth  or  fifth  day,  it 
is  a  sign  of  an  extension  or  inflammatory  reaction  of  the  hemorrhage. 
Hence  the  thermometer  furnishes  a  very  important  criterion  of  the 
seriousness  of  the  case. 

The  varying  course  of  the  apoplexy  is  shown  in  the  foUowing  diagram: 

Health  line 


'  3.  Chronic  stage. 

Improvement  .\ 


Attack. 


1.  Death. 
2  to  4  days.  2.  Death. 

2  to  4  weeks. 

The  Chronic  Stage,  Hemiplegia. — The  description  of  this  condition 
applies  almost  equally  to  all  forms  of  apoplexy  with  hemiplegia.  At 
the  end  of  a  month,  if  fever  and  symptoms  of  cerebral  irritation  have 
subsided,  the  chronic  stage  may  be  said  to  begin.  The  hemiplegia 
has  improved,  the  patient  can  move  the  leg  and  arm  a  little,  sensory 
symptoms  have  lessened,  the  mind  is  clear,  headache  has  disappeared. 
Improvement  continues,  though  more  slowly,  for  several  months  or  even 
one  or  two  years.     During  this  time  the  patient  is  "a.  hemiplegic." 

The  hemiplegia  affects  the  arm  more  than  the  leg,  and  the  face  least 


428 


DISEASES    OF    THE    NERVOUS    SYSTEM 


of  all.  The  distal  segments  of  the  limbs,  the  feet  and  hands,  are  af- 
fected more  than  those  near  the  trunk.  The  muscles  that  act  bilater- 
ally, such  as  those  of  respiration,  phonation,  and  facial  expression, 
are  but  shghtly  involved.  The  paralysis  is  not  strictly  a  hemiplegia, 
for  the  muscles  on  the  sound  side  are  somewhat  weakened,  as  tests  will 
show.  In  severe  cases,  especially  in  old  people,  even  the  visceral  muscles, 
especially  those  of  the  bladder,  are  weakened.  At  the  onset  of^the 
attack  there  is  sometimes  a  temporary  ''initial"  rigidity  of  the  muscles 
on  the  paralyzed  side,  or  an  "early"  rigidity  may  develop  in  one  or  two 
daj'^s.  There  always  develops  at  about  the  beginning  of  the  second 
week  a  "late"  rigidity.  This,  which  at  first  is  slight,  gradually  increases, 
and  finally  contractures  affect  the  paralyzed  limbs.  The  superficial 
reflexes,  which  at  first  were  absent  rarely  reappear;  the  tendon  reflexes 


Fig.  210. — Showing  athetoid  movements  of  hands.     (Curschmann.) 


become  much  exaggerated,  and  clonus  can  be  obtained  in  the  leg  and 
arm.  The  sound  side  shares  to  a  small  extent  in  these  conditions.  The 
contractures  affect  the  extensors  of  the  foot  more  than  the  flexors,  and 
bring  the  toe  down  and  the  heel  up.  The  leg  is  held  nearly  extended, 
and  the  limb  in  walking  is  swung  around,  the  toe  scraping  the  ground. 
The  shoulder  is  adducted,  the  forearm  flexed,  and  the  fingers  are  tightly 
shut  into  the  palm  by  the  overaction  of  the  flexors  (Fig.  209).  The  facial 
muscles  show  a  slight  contraction  and  drawing  to  the  affected  side.  The 
muscles  on  the  paralyzed  side  do  not  waste.  In  infantile  hemiplegia, 
however,  the  affected  limbs  grow  less  than  those  on  the  sound  side. 

The  paralyzed  limbs  may  be  the  seat  of  peculiar  disorders  of  move- 
ment.    These  consist  of: 

Associated  movements,  tremor,  ataxia,  choreic  movements,  continu- 


DISEASES    OF    THE    BRAIN  429 

ous  or  athetoid  movements  (Fig.  210),  spastic  movements  and  cramps. 

Such  movements,  aside  from  those  that  are  spastic,  are  rarely  seen 
in  the  hemiplegia  of  adults. 

The  electrical  irritability  may  be  at  first  shghtly  increased  or  di- 
minished, but  the  change  is  small  in  amount  and  never  reaches  the 
degenerative  stage.  The  direct  muscular  irritabilit}'-  is  at  first  increased 
on  the  affected  side. 

Hemiansesthesia,  if  present  at  first,  disappears  to  a  great  extent, 
leaving  only  residua  about  the  feet  and  hands.  Parsesthesise  are  com- 
mon. In  rare  cases  the  patient  suffers  great  pain  in  the  arm  and  leg. 
This  pain  is  generally  of  a  neuralgic  or  burning  character  and  very 
obstinate  and  distressing.  Cramping  pains  in  the  legs  and  arms  are 
common  in  the  severer  cases. 

During  the  first  few  weeks  after  the  onset,  the  temperature  of  the 
hemiplegia  side  is  usually  a  very  little  higher  than  that  of  the  sound  side. 

Vasomotor  disturbances,  sweating,  skin  eruptions,  and  increased 
growth  of  hair  are  some  of  the  rarer  symptoms. 

The  mental  condition  is  sometimes  affected.  The  patient  becomes 
irritable,  cries  easily,  and  is  in  general  more  emotional.  The  memory 
is  impaired,  and  the  power  of  concentrating  the  attention  and  carrying 
on  work  is  less.  Sometimes  a  progressive  mental  deterioration  sets  in 
and  epilepsy  or  insanity  develops.  The  mental  disturbance  is  greater 
in  old  people  and  depends  somewhat  on  the  size  of  the  hemorrhage. 
Those  forms  which  produce  serious  aphasia  especially  limit  and  lessen 
mental  activity. 

Dural  Hemorrhages. — Hemorrhages  from  the  vessels  of  the  dura 
mater  are  usually  due  to  a  rupture  of  the  middle  meningeal  artery  or 
vein  or  some  of  the  cerebral  veins  as  they  pass  to  the  sinus,  and  this  is 
especially  true  in  such  hemorrhages  as  are  the  result  of  injuries  to  the 
head.  The  causes  are  blows  on  the  head,  obstetrical  injuries,  alcoholism, 
and  the  dementias. 

In  dural  hemorrhages  the  result  of  blows  on  the  head,  the  clot  is  some- 
times intra-dural,  lying  in  the  arachnoid  space,  and  sometimes  epidural, 
lying  between  the  bone  and  the  dural  membrane.  The  extra-dural 
hemorrhages  are  perhaps  a  little  more  common  in  surgical  experience; 
the  intra-dural  in  medical  and  especially  asylum  experience.  In  over 
one-half  of  extra-dural  cases  there  is  an  interval  of  consciousness  lasting 
from  a  few  hours  to  two  months,  but  usually  only  a  few  hours,  between 
the  accident  and  the  time  when  distinctive  cerebral  symptoms  de- 
velop. Then  the  patient  gradually  becomes  dull,  somnolent,  and 
finally  comatose.  Along  with  the  gradual  or  rather  sudden  loss  of  con- 
sciousness there  develops  a  hemiplegia  upon  the  side  opposite  the  clot. 
This  is  usually  not  complete,  though  it  may  become  so.     It  is  much  less 


430  DISEASES    OF   THE    NERVOUS    SYSTEM 

common  in  extra-dural  hemorrhage.  Anaesthesia  is  rarely  present.  The 
reflexes  are  generally  somewhat  exaggerated,  and  there  may  be  consider- 
able rigidity.  Spasmodic  movements  of  some  kind  occur  in  nearly  half 
the  extra-dural  cases  and  in  more  than  half  of  the  intra-dural.  These 
spasmodic  movements  may  involve  the  whole  of  the  affected  side,  or 
may  simply  affect  the  eyes  and  the  facial  muscles.  They  consist  of 
irregular  twitchings.  The  pupils  are  usually  somewhat  contracted, 
more  so  upon  the  paralyzed  side.  When  there  is  a  dilated  pupil  on  the 
side  of  the  lesion  and  a  small  pupil  on  the  opposite  side,  it  is  known  as 
the  Hutchinson  pupil,  and  means  a  severe  brain  compression  involving 
the  third  nerve  at  the  base.  The  eyes  are  generally  both  turned  toward 
the  affected  side  and  away  from  the  lesion.  The  pulse  is  hard,  slow  and 
full;  the  tension  high;  the  respiration  is  rarely  stertorous,  though  it  may 
sometimes  be  so,  and  Cheyne-Stokes  respiration  may  be  present.  In 
these  cases  the  clot  is  very  large  and  the  compression  great.  Aphasia 
may  be  present  if  the  clot  is  upon  the  left  side.  The  temperature  may 
be  raised  one  or  two  degrees,  or  it  may  be  normal.  The  progress  of  the 
disease  is  usually  steadily  fatal  unless  surgical  interference  is  undertaken. 
The  coma  deepens,  the  respiration  becomes  stertorous  and  then  embar- 
rassed, the  pulse  gets  rapid  and  weak,  and  the  patient  dies.  With 
surgical  interference  (since  1886),  between  two-third  and  three-fourths 
of  the  cases  are  saved  (Scudder  and  Lund). 

Subdural  hemorrhages  not  caused  by  injuries  are  due  sometimes  to 
the  rupture  of  a  meningeal  artery,  but  usually  to  rupture  of  the  veins  of 
the  pia  mater  or  to  the  rupture  of  new  vessels  formed  in  a  pachymeningeal 
exudate.  This  spontaneous  hemorrhage  is  rare  iii  ordinary  practice,  but 
is  not  specially  so  in  insane  asylums  or  in  large  city  hospitals.  This  is  be- 
because  the  two  great  causes  of  this  type  of  hemorrhage  are  the  dementias 
and  alcoholism.  General  paresis  is  the  form  of  insanity  with  which  it  is  of- 
tenest  associated.  In  the  case  of  alcohohcs,  it  is  probable  that  injuries  from 
blows  are  an  exciting  factor  in  the  production  of  the  hemorrhage,  these 
occurring  while  the  patient  is  in  a  state  of  intoxication.  The  symptoms 
of  these  hemorrhages  are  extremely  variable,  owing  to  the  complicating 
influences  of  the  insanity  and  alcohol.  The  patient,  after  suffering  from 
headaches  or  vertigo,  becomes  suddenly  comatose  and  shows  marked 
evidences  of  hemiplegia  and  even  of  hemiansesthesia.  Rigidity  of  the 
paralyzed  side  is  often  present,  and  sometimes  spasmodic  movements  are 
observed.  On  the  other  hand,  at  times  the  paralysis  can  hardly  be  ob- 
served, and  the  patient  is  in  a  semicomatose  state,  has  a  muttering 
delirium,  and  presents  the  general  aspect  of  a  person  suffering  from  the 
oedema  or  "wet-brain"  of  alcoholics.  In  dural  hemorrhages  occurring  in 
paresis,  the  patient  usually  without  warning  becomes  unconscious,  and 
he  often  has  some  convulsive  symptom  and  a  hemiplegia  develops.     In 


DISEASES    OF    THE    BRAIN  431 

these  cases  there  is  often  a  rapid  improvement,  and  the  patient  gets 
partly  well,  usually  experiencing  other  attacks  later. 

Pial  Hemorrhages. — Hemorrhages  from  the  pial  arteries  are  rare 
and  of  small  extent. 

The  most  frequent  cause  is  trauma,  associated  perhaps  with  syphilis 
and  alcoholism.  In  many  instances  very  slight  localizing  symptoms 
occur,  and  no  absolute  diagnosis  can  be  made.  If  the  hemorrhage, 
however,  is  in  the  motor  area  of  the  cortex,  local  spasmodic  movements 
and  some  hemiplegia  are  observed.  The  most  characteristic  symptoms 
are  the  sudden  incomplete  hemiplegia,  involving,  perhaps,  mainly  an  arm 
or  a  leg,  associated  with  local  spasmodic  movements,  resembhng  Jack- 
sonian  epilepsy. 

Hemorrhages  due  to  rupture  of  large  pial  veins  occur  most  often  as 
obstetrical  injuries.  The  hemorrhages  here  may  cause  convulsions, 
paralysis  and  death,  or  lead  to  permanent  mental  and  physical  defects. 

Hemorrhages  of  the  Vertebral  Artery  and  its  Branches. — Hemorrhage 
in  the  medulla  is  extremely  rare.  If  of  any  size,  it  causes  instant  death; 
if  small,  it  will  leave  symptoms  similar  to  those  of  softening. 

Hemorrhage  of  the  'pons  is  also  rare,  but  it  makes  up  2  per  cent. 
of  my  cases.  The  cause  is  much  the  same  as  that  for  cerebral  hemor- 
rhages, though  syphilis  is  less  often  a  factor.  In  nearly  half  the  cases 
the  hemorrhage  is  a  large  and  immediately  fatal  one.  In  the  majority 
of  cases  it  is  a  small  focal  hemorrhage  from  rupture  of  a  transverse  or 
median  branch  of  the  basilar  artery. 

The  patient  has  some  prodromal  headaches  and  malaise  for  a  few 
days,  with  vertigo  and  sometimes  vomiting.  Then  he  falls  suddenlj^ 
as  if  by  a  lightning  stroke,  into  a  coma,  usually  very  profound.  There 
are  twitchings  of  the  face  or  of  the  limbs  or  both,  but  rarely  any  general 
convulsion  (three  cases).  The  face  is  flushed,  there  is  a  fall  of  tem- 
perature and  the  pulse  is  irregular,  but  not  markedly  increased  or 
slowed;  as  a  rule,  the  respiration  is  slow,  4  or  6  per  minute,  or  more 
often  irregular,  and  of  Cheyne-Stokes  type.  The  pupils  are  con- 
tracted to  a  pin-point,  and  do  not  respond  to  light,  but  may  be  uneven. 
There  is  convergent  strabismus  or  conjugate  deviation  of  the  eyes. 
The  limbs  are  at  first  stiff,  but  may  be  relaxed  later  and  the  reflexes 
increased. 

The  patient  cannot  be  aroused,  but  can  be  made  to  vomit.  A  few 
hours  later  the  temperature  rises,  sometimes  very  high — 106  to  108 — 
but  usually  not.  There  are  involuntary  movements  of  the  bowels, 
swallowing  is  impossible;  evidences  of  dyspnoea  are  shown.  The  pulse 
becomes  more  rapid,  cyanosis  develops,  the  patient  dies  in  six  to  twenty 
hours,  usually  with  evidence  of  paralysis  of  respiration. 

If  the  hemorrhage  is  less  severe,  the  coma  is  less  profound  or  may 


432  DISEASES    OF    THE    NERVOUS    SYSTEM 

be  absent,  the  patient  shows  signs  of  agonizing  suffering  and  difficulty 
in  respiration,  evidences  of  crossed  paralysis,  crossed  anaesthesia;  and 
disturbance  of  equilibrium  and  ataxia  can  be  noted. 

In  still  smaller  lesions  we  find  no  such  severe  general  symptoms, 
but  only  those  due  to  a  circumscribed  focus  in  one  side  of  the  pons, 
because  the  smaller  lesions  are  unilateral.  The  syndrome  of  serious  pons 
lesions  then  is : 

1.  Headache,  malaise,  vomiting. 

2.  Sudden  and  profound  coma. 

3.  Twitching  of  the  face  and  limbs  or  both. 

4.  Myosis  and  convergent  strabismus  or  conjugate  deviation  (away 
from  the  side  of  the  lesion) . 

5.  Slow,  irregular  breathing. 

6.  Irregular  pulse. 

7.  Dysphagia. 

8.  Paratysis  of  limbs  or  crossed  paralysis  and  exaggerated  reflexes. 

9.  Gradual  rise  of  temperature,  sometimes  to  high  point. 

10.  Death  inside  of  twenty-four  hours. 

Cerebellar  Apoplexy. — Hemorrhage  into  the  cerebellum  occurs  in 
1  or  2  per  cent,  of  all  fatal  cases.  Its  recognition  is  very  difficult. 
There  is  sometimes  a  preliminary  period  of  severe  headache,  lasting 
several  days.  In  other  cases  the  patient  at  once  falls  into  a  state  of 
profound  coma,  with  stertorous  respiration.  Vomiting  sometimes 
occurs.  There  may  be  some  hemiplegia,  and  if  so  this  is  on  the  side  of 
the  lesion,  owing  to  this  pressure  on  the  motor  tract.  Distinct  evidences 
of  hemiplegia,  however,  are  not  always  observed.  The  condition 
of  the  pulse  and  arterial  system  is  very  much  like  that  of  ordinary 
apoplexy,  but  the  respiratory  system  is  usually  more  seriously  affected. 
Disturbances  in  the  movements  of  the  eyes  and  in  swallowing,  and  in 
fact  all  those  symptoms  which  show  a  pressure  or  irritation  due  to  blood 
oozing  into  the  fourth  ventricle  may  be  present.  Death  is  almost  sure 
to  occur,  and  is  inevitable  if  the  hemorrhage,  as  is  so  often  the  case, 
breaks  through  and  reaches  the  fourth  ventricle. 

If  the  hemorrhage  is  small  and  does  not  break  into  the  ventricle, 
the  patient  suffers  from  intense  vertigo  which  obliges  him  to  lie  per- 
fectly still  in  a  horizontal  position.  With  or  preceding  this  he  may 
fall  down  and  have  convulsive  movements  or  forced  and  irregular  tonic 
contractions  of  the  muscles;  in  other  words,  a  cerebellar  fit.  If  this 
passes  away  the  vertigo  also  may  pass,  and  the  patient  gets  nearly 
well,  but  is  left  with  some  feeling  of  uncertainty  in  gait,  and  with  tinnitus 
cerebri  and  tendency  to  vertiginous  and  cerebellar  attacks. 

Pathology  and  Morbid  Anatomy. — Spontaneous  intra-cranial  hemor- 
rhage is  always  due  to  the  presence  of  diseased  blood-vessels  in  the  brain. 
This  diseased  condition  consists  of: 


DISEASES    OF    THE   BRAIN  433 

1.  A  degenerative  arteritis  which  results  sometimes  in  producing  small 
aneurisms.  2.  A  fatty  degeneration  of  the  vessel  walls.  3.  Besides 
this,  in  most  cases  the  larger  blood-vessels  are  atheromatous. 

The  arteritis  may  produce  small  or  miliary  aneurisms  which  involve 
only  the  smaller  arteries,  especially  those  of  the  central  group.  They 
may  be  fusiform  or  sacculated  in  shape;  they  range  in  size  from  one- 
fourth  to  one  millimetre  (Koo  to  3^^5  in.)  in  diameter.  They  are  usually 
not  very  numerous,  but  there  may  be  as  many  as  a  hundred  in  the 
brain.  They  are  the  results,  not  of  inflammation,  but  of  a  degenera- 
tion which  affects  first  an  area  in  the  internal  coat;  this  causes  local 
weakness  and  consequent  dilatation;  secondarily  there  is  a  peri-arteritis. 
These  aneurisms  occur  almost  exclusively  during  the  degenerative 
period  of  life. 

Fatty  degeneration  of  the  walls  of  the  small  cerebral  arteries  occurs 
in  purpura,  scurvy,  marasmic  conditions,  and  post-infective  states,  especi- 
ally in  early  life,  and  is  the  common  cause  of  hemorrhage  at  that  time. 

Atheroma  affects  the  larger  vessels  only.  It  is  indirectly  a  cause  of 
hemorrhage  by  lessening  the  elasticity  of  the  vessel  wall.  Atheroma 
is  present  in  from  one-eighth  to  one-fifth  of  all  cases.  Hypertrophy  of 
the  heart  is  a  factor  in  causing  hemorrhage,  and  such  hypertrophy  exists 
in  about  40  per  cent,  of  cases.  Emboli  lodged  in  the  cerebral  arteries 
may  cause  hemorrhage  by  suddenly  stopping  the  arterial  circulation  and 
raising  the  blood-pressure.  Hemorrhages  are  found  by  far  the  oftenest 
(20  per  cent.)  in  the  caudate  and  lenticular  nuclei  and  adjacent 
parts.  The  lenticular  and  lenticulo-striate  branches  of  the  middle  cere- 
bral are  oftenest  affected;  next  the  branches  of  the  anterior  cerebral 
to  the  caudate  nucleus  and  the  lenticulo-optic  branches  of  the  middle 
cerebral.  The  branches  of  the  posterior  cerebral  break  more  rarely. 
The  parts  affected  in  hemorrhage  in  fatal  hospital  cases,  in  order  of 
frequency,  are  about  as  follows  (Hoobler). 


Frontal  lobe 

24 

Parietal  lobe 

14 

Occipital  lobe 

6 

Temporal  lobe 

14 

Corpus  striatum 

62 

Optic  thalamus 

25 

Internal  capsule 

28 

Ventricles 

64 

Corpus  callosum 

1 

Corpora  quadrigemina 

1 

Pise  and  cortical 

8 

Pachymeningeal 

7 

Pons 

1 

Cerebellum 

3 

28 


258 


434  DISEASES    OP    THE    NEEVOUS    SYSTEM 

These  figures  show  that  over  three-fourths  of  all  the  hemorrhages 
occur  from  rupture  of  the  central  or  ganglionic  arteries. 

Cortex  hemorrhages  are  generally  small  and  may  be  subarachnoid 
or  may  break  through  into  the  arachnoid  cavity.  Ventricular  hemor- 
rhages are  almost  always  secondary  to  a  rupture  into  the  neighborhood 
of  the  basal  ganglia.  Pons  hemorrhages  occur  usually  in  the  median 
line.  Cerebellar  hemorrhages  are  oftenest  due  to  rupture  of  the  superior 
cerebellar  artery.  They  usually  cleave  their  way  externally  and  break 
into  the  fourth  ventricle.  Dural  hemorrhages  are  due  to  rupture  of  the 
meningeal  veins  and  arteries  and  of  the  vessels  in  newly  organized  clots. 
They  lie  in  the  arachnoid  cavity  and  flatten  the  convolutions. 

The  reparative  changes  after  a  hemorrhage  take  the  following  course : 
1st.  Coagulation  of  the  blood,  which  in  a  few  days  begins  to  soften 
and  become  absorbed.  2d.  Formation  of  a  fibrinous  wall  about  the 
clot.  This  occurs  from  the  seventh  to  the  ninth  day.  3d.  Formation 
of  a  cyst  with  transparent  fluid  contents,  and  perhaps  fibrous  trabeculse 
running  through  it,  twentieth  to  thirtieth  day.  4th.  Contraction 
of  the  cyst  wall,  which  begins  by  the  fortieth  day.  5th.  Secondary 
degenerations  begin  from  the  tenth  to  the  fourteenth  day.  These  de- 
generations vary  with  the  location  of  the  lesion.  The  most  important 
one  is  that  of  the  pyramidal  tract.  This  is  more  or  less  completely 
sclerosed  from  the  lesion  to  the  spinal  cord. 

The  diagnosis  of  hemorrhagic  apoplexy  must  be  made  from  al- 
coholic coma,  ursemic  coma,  diabetic,  opium  and  other  types  of  coma, 
epilepsy  and  hysteria;  acute  softening  from  embolism  and  thrombosis. 

From  alcoholic  coma  the  diagnosis  is  made  by  the  odor  of  the  breath, 
the  incomplete  coma,  the  equal  pupils,  the  absence  of  low  or  unequal 
temperature,  the  absence  of  paralysis,  the  equality  of  the  reflexes. 

From  ursemic  coma  by  the  presence  of  albumin  and  casts  in  the  urine, 
though  their  presence  does  not  surely  indicate  ursemia;  by  the  equal 
pupils,  the  temperature,  the  absence  of  hemiplegia  and  the  presence 
of  the  physiognomy  peculiar  to  cases  of  chronic  Bright's  disease. 

From  diabetic  coma  by  the  odor  of  the  breath  and  the  condition  of 
the  urine. 

From  opium  poisoning  by  the  history,  the  stomach  contents,  the 
presence  of  equal  and  contracted  pupils,  the  slow  respirations,  the 
temperature,  and  the  absence  of  paralysis. 

From  epilepsy  by  the  history  of  the  onset  with  epileptic  cry,  the 
dilated  and  equal  pupils,  the  biting  of  the  tongue,  the  absence  of  hemi- 
plegia, the  rather  rapid  return  of  consciousness. 

Hysterical  attacks  present  little  semblance  to  that  of  apoplexy; 
consciousness  is  not  profoundly  lost;  the  deep  and  superficial  reflexes 
are  not  greatly  changed;  the  hemiplegia  is  characterized  by  its  flaccidity, 


DISEASES    OF    THE    BRAIN  435 

by  its  not  involving  the  face,  and  by  the  presence  of  the  ansesthesias 
and  other  hysterical  stigmata.^ 

In  embolic  softening  the  earlier  age  of  the  patient,  the  presence 
of  decided  valvular  heart  disease,  the  parturient  condition,  the  slighter 
degree  and  shorter  duration  of  coma,  the  absence  of  serious  disturbance 
of  temperature,  the  onset  first  of  paralysis  and  then  of  convulsive  move- 
ments and  coma — all  lead  to  a  presumption  in  favor  of  embolism. 

The  presence,  on  the  other  hand,  of  a  congested  face,  tense  pulse, 
and  throbbing  carotids  favors  the  existence  of  a  hemorrhage. 

From  thrombotic  softening  diagnosis  is  more  difficult.  The  exist- 
ence of  syphilis  is  in  favor  of  thrombosis.  The  occurrence  of  pro- 
dromata,  consisting  of  slight  seizures  quickly  recovered  from,  the  slighter 
degree  of  coma,  the  advanced  age,  hard  atheromatous  arteries,  low 
blood-pressure,  evidence  of  ansemia  and  asthenia,  weak  or  fatty  heart, 
the  absence  of  stertorous  respiration,  flushed  face,  and  unequal  tem- 
perature not  much  lowered  or  raised,  the  slight  pupillary  disturbance, 
and  absence  of  convulsions  point  to  thrombotic  softening.  Evidence 
of  a  lesion  in  the  pons  or  cerebellum  unless  there  is  syphilis  suggests 
hemorrhage,  while  evidence  of  lesion  in  the  medulla  points  almost  surely 
to  softening.  The  existence  of  a  very  high  blood-pressure  will  often  help 
the  diagnosis  in  all  cases,  but  especially  from  softenings. 

Several  authors  have  found  large  granular  macrophages  containing 
red  blood-cells  in  the  cerebrospinal  fluid  in  cerebral  hemorrhage,  but 
these  are  not  always  found  (Hastings).  The  examination  of  the  urine 
for  haemoglobin  has  also  been  used  as  a  diagnostic  test. 

Lumbar  puncture  and  the  finding  of  blood  in  the  cerebro-spinal 
fluid  indicate  a  ventricular  or  surface  hemorrhage. 

The  chances  in  any  case  between  the  ages  of  thirty  and  fifty,  in  a  city 
hospital  practice,  if  there  is  no  heart  disease,  are  six  to  one  in  favor  of 
hemorrhage,  if  syphilis  can  be  excluded. 

The  diagnosis  of  the  location  of  the  lesion  has  already  been  indicated, 
except  for  the  central  hemorrhages.     These  represent  four  clinical  types: 

1.  That  due  to  rupture  of  the  lenticulo-striate  branch  of  the  middle 
cerebral  with  injury  of  the  lenticular  region  and  internal  capsule  in  its 
more  anterior  part.  This  gives  the  picture  of  the  usual  type  of  hemiplegia 
as  described  with  no  marked  sensory  symptoms. 

2.  If  the  lenticulo-optic  is  involved,  there  is  less  hemiplegia  and  the 
leg  is  more  involved,  and  there  is  involvement  of  sensation. 

'^  Hoover's  sign  of  hemiplegia:  The  patient  lies  on  his  back.  The  examiner 
places  his  hand  under  the  patient's  heel  on  the  side  of  the  paralysis  and  directs  him 
to  lift  the  sound  leg.  In  an  organic  hemiplegia  the  examiner  feels  that  the  patient's 
heel  presses  down  against  his  hand,  when  the  patient  lifts  the  sound  leg.  This  does 
not  occur  in  hysterical  hemiplegia,  nor  upon  lifting  the  paretic  leg,  nor  in  the  normal 
subject. 


436 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


3.  If  the  thalamic  arteries  are  involved,  there  is  a  temporary  hemi- 
plegia with  appearance  of  the  thalamic  syndrome. 

4.  Ventricular  hemorrhages  are  usually  the  result  of  very  extensive 
lenticulo-striate  lesions,  the  blood  finally  bursting  into  a  lateral  ventricle 
and  thence  permeating  into  all  the  ventricles  and  even  to  the  subarach- 
noid space,  so  that  a  diagnosis  can  be  made  or  confirmed  by  a  lumbar 
puncture.  The  symptoms  are  characterized  by  the  severity  of  the  coma, 
giving  way  of  the  medullary  centres,  a  motor  restlessness,  increased 
rigidity  of  the  limbs,  and  sometimes  evidence  of  bilateral  paralysis. 
The  contracted  pupils,  loss  of  power  over  the  sphincters,  sweating, 
vasomotor  disturbances,  rise  of  temperature,  irregular  respirations,  and 


Poster!  oi 

communicatin" 

Antei'ior  choroi  <  I 

Post,  cerebral 


1^ V    \     /'■"^""/i/-yfr/y,>r A. 


Fig.  211. — Blood-supply  of  basal  ganglia  and  internal  capsule.     {Bing.) 


rapid  pulse  indicate  a  serious  cerebral  lesion.  The  blood-pressure, 
which  is  high  when  there  is  a  large  clot  on  the  brain  substance,  falls  if  it 
breaks  into  the  ventricles. 

Prognosis. — The  majority  of  cases  apparently  get  over  the  first  attack 
of  apoplexy,  but  it  is  possible  that  many  of  these  cases  are  thrombotic 
rather  than  hemorrhagic.  My  view,  however,  is  that  since  the  majority 
of  hospital  cases  recover  and  since  the  majority  of  these  are  hemorrhagic 
there  is  a  large  number  of  recoveries.  They  are  very  liable  to  have  an- 
other within  one  to  five  years.  The  minority  recover  from  this.  Few 
survive  a  third  attack.  The  prognosis  of  the  attack  itself  depends  on  the 
severity  of  the  coma  and  paralysis,  the  disturbance  of  temperature  and  of 


DISEASES    OF    THE   BRAIN 


437 


respiration,  the  evidence  of  rupture  into  the  ventricles,  the  development  of 
decubitus,  the  continuance  of  loss  of  control  over  the  bowels  and  bladder. 

If  profound  coma  continues  four  days  there  is  little  hope;  if  fever 
develops  and  continues  steadily,  or  if  there  is  initial  subnormal  tempera- 
ture, or  if  signs  of  bulbar  compression  and  paralysis  occur,  the  progonosis 
is  grave. 

If  the  patient  passes  the  first  week  with  little  or  no  fever  and  con- 
sciousness has  returned,  the  prognosis   is 
good. 

The  presence  of  renal  disease  and  of 
alcoholism  is  bad.  Development  of  slight 
delirium  which  continues  is  unfavorable. 

Cerebellar  and  pons  hemorrhages  are 
very  fatal,  meningeal  less  so. 

The  prognosis  of  the  chronic  stage  has 
been  given  under  symptoms. 

Improvement  continues  rather  rapidly 
for  three  months,  then  very  slowly.  Im- 
provement may  continue  for  one  or  two 
years.  Complete  recovery  is  very  rare. 
The  great  danger  after  middle  age  is  recur- 
rence of  the  attack. 

Something  of  the  course  of  the  apo- 
plexies in  a  large  city  hospital  is  shown  by 
the  following  statistics: 

In  three  recent  years  there  were  ad- 
mitted to  Belle vue  Hospital  315  cases  of 
cerebral  apoplexy  with  hemiplegia.  Of 
these,  115  died  and  of  these  26  were 
autopsied.  In  10  cases  the  hemorrhage 
involved  the  central  arteries  and  broke 
into  the  lateral  ventricles.  In  16  the  len- 
ticular region  and  capsule  only  were  in- 
volved. 

Treatment  of  the  Attack. — The  patient 
should  be  laid  in  a  horizontal  position  and  kept  quiet.  Ice  may  be 
applied  to  the  head  and  hot  bottles  at  the  feet,  only  if  these  measures 
seem  indicated.  They  usually  do  no  good.  A  laxative  should  be  given, 
either  one  or  two  drops  of  croton  oil  or  a  quarter  of  a  grain  of  elaterium. 
If  there  is  evidence  of  intense  cerebral  congestion,  the  pulse  being  very 
full  and  hard  and  the  heart  beating  strongly  and  blood-pressure  high, 
bleeding  eight  to  twelve  ounces  is  justifiable.  Ordinarily  it  is  better  to 
give  tincture   of  aconite  every  twenty  minutes  for  two  or  three  hours. 


Fig.  212 . — D  i  a  g  r  a  m  m  a  t  i  c 
representation  of  the  internal 
capsule  and  the  cortical  tracts 
that  pass  through  it.  1,  2, 
Fronto-occipito-pontine  efferent; 
a,  V,  auditory,  visual,  afferent; 
F,  cortico-spinal  from  face  center; 
H,  hand;  A,  arm;  B,  leg;  *S,  sen- 
sory tract.  {Bing.)  C,  T,  L, 
and  the  internal  capsule  are  the 
parts  most  often  involved  in 
hemorrhage. 


438  DISEASES    OF    THE    NEKVOUS    SYSTEM 

Administration  of  bromide  of  sodium  and  enemata  of  ergot  have  been 
advised,  but  are  of  doubtful  value.  After  the  first  twelve  hours,  treat- 
ment must  be  symptomatic.  Should  delirium  and  other  evidence  of 
mental  irritation  appear,  chloral  hydrate  or  morphine  and  hyoscin  are 
indicated,  and  an  elaterium  purge,  given  if  the  patient  is  not  too  weak. 
The  use  of  iodide  of  potassium  or  mercury  is  not  indicated  unless  the 
case  is  distinctly  syphilitic.  Great  care  should  now  be  taken  that  the 
patient  does  not  develop  pneumonia.  The  mouth  and  pharynx  should 
be  cleansed  antiseptically,  and  the  patient  should  not  be  allowed  to  re- 
main in  one  position.  If  there  is  sufficient  evidence  of  a  meningeal  or 
cortical  clot,  trephining  should  be  seriously  considered. 

At  the  end  of  three  or  four  weeks  or  even  earlier  careful  massage 
should  be  begun  and  continued  daily.  With  it  the  faradic  battery  may 
be  used  on  the  affected  limbs.  When  contractures  develop  the  stabile 
galvanic  current  may  be  tried,  though  it  does  little  good.  Static  sparks, 
however,  are  helpful;  lukewarm  baths  should  be  tried  and  measures 
used  to  produce  a  hyperextension  of  the  affected  parts. 

Internally  during  this  time  the  patient  is  to  be  given  courses  of 
iodide  of  potassium,  tonics,  and  laxatives  if  needed.  The  patient  should 
be  made  to  live  a  quiet  life,  preferably  in  a  warm,  equable  climate. 
The  kidneys  should  be  kept  active  and  arterial  tension  only  moderately 
low.  For  these  purposes  nitroglycerine  should  be  given  and  at  times 
small  doses  of  chloral,  and  the  diet  should  be  simple  and  rather  non- 
nitrogenous.  Strychnine  in  very  small  doses  (gr.  Hoo)  sometimes  helps 
the  contractures,  as  also  do  the  bromides  and  phj^sostigma. 

APOPLEXY  FROM  ACUTE  SOFTENING 

{Embolism,  Thrombosis) 

Acute  softening  is  a  condition  caused  by  the  plugging  of  a  blood- 
vessel with  an  embolus  or  thrombus,  and  is  characterized  by  a  com- 
paratively sudden  (embolism),  or  gradual  (thrombus),  apoplectic  seizure, 
the  symptoms  eventually  running  a  course  much  like  that  of  cerebral 
hemorrhage. 

Etiology. — Embolism  occurs  rather  more  often  in  women,  throm- 
bosis in  men.  Embolism  is  rare  in  children;  it  occurs  oftenest  between 
the  ages  of  twenty  and  fifty,  thrombosis  between  the  ages  of  fifty  and 
seventy.  The  most  important  predisposing  factors  in  embolism  are 
acute  or  recurrent  endocarditis,  infectious  fevers,  profound  anaemia, 
pregnancy,  and  blood  dyscrasias;  in  thrombosis,  arterial  sclerosis  from 
any  cause.  Severe  gas  poisoning  leads  sometimes  to  thromboses.  The 
same  causes  which  lead  to  the  arterial  disease  which  produces  cere- 
bral hemorrhage  also  predispose  to  thrombosis,  though  in  the  latter 
condition  atheroma  and  obliterating  arteritis  play  the  important  part. 


DISEASES    OF    THE    BEAIN  439 

Symptoms. — In  embolism  there  are  rarely  any  premonitory  symp- 
toms; the  onset  is  sudden;  it  may  begin  with  some  convulsive  twitch- 
ings,  then  follow  hemiplegia  and  temporary  loss  of  consciousness.  Coma, 
however,  is  rarer  than  in  hemorrhage,  and  if  present  is  usually  shorter. 
There  is  rarely  vomiting,  nor  do  we  find  the  hard,  pulsating  arteries, 
flushed  face,  and  severely  stertorous  breathing.  The  initial  temperature 
changes  are  slight,  but  in  a  few  days  fever  may  develop. 

In  thrombosis  premonitory  symptoms  are  frequent.  In  syphilitic 
cases  there  are  headaches  and  cranial-nerve  palsies.  In  these  and  other 
cases  vertigo,  temporary  aphasia,  insomnia,  transient  hemiplegia,  numb- 
ness of  the  hand  and  foot,  and  drowsiness  may  be  present.  The  onset  is 
more  gradual;  the  hemiplegia  slowly  develops,  taking  several  hours, 
or  days  and  coming  on  with  remissions,  finally  the  patient  gradually 
becomes  completely  hemiplegic  often  without  coma.  The  attack  some- 
times is  rather  sudden,  with  no  loss  of  consciousness,  and  it  may  occur 
in  sleep.  The  temperature  often  has  a  sHght  initial  fall,  f oUowed  by  a 
rise,  just  as  in  hemorrhage.  In  both  embolism  and  thrombosis  the  hemi- 
plegia tends  to  improve  very  much  in  a  few  days  or  weeks  unless  the 
vessel  obliterated  is  a  large  one.  Embolism  is  rather  more  apt  to  affect 
the  left  side  of  the  brain,  though  the  difference  is  not  great.  The  middle 
cerebrals  are  most  frequently  affected.  Thromboses  affect  the  vertebrals, 
basilar,  and  posterior  cerebral  arteries  more  often  relatively  than  do 
hemorrhages;  then  the  initial  symptoms  may  not  present  the  character 
of  hemiplegia,  but  of  a  ponto-bulbar  paralysis  or  sensory  hemiplegia. 
Acute  softening  may  kill  within  twenty-four  hours,  but,  as  a  rule,  the 
patient  survives  the  onset,  and  if  he  dies  it  is  not  for  several  weeks.  After 
the  acute  stage  is  over  the  patient  passes  into  the  chronic  stage,  which 
resembles  in  nearly  all  respects  that  of  hemorrhage.  After  an  acute 
softening,  however,  it  is  believed  that  there  are  more  spastic  symptoms 
and  a  greater  tendency  to  mobile  spasm.  In  embolism,  owing  to  the 
youth  and  freedom  from  arterial  disease,  the  mind  is  less  affected;  while  in 
thrombosis  the  contrary  is  the  case. 

In  acute  softening  from  gas-poisoning,  a  branch  of  the  anterior 
cerebral  artery  which  supplies  the  caudate  and  part  of  the  lenticular 
nuclei  is  particularly  affected  so  that  a  symmetrical  softening  of  both 
lenticular  nuclei  is  almost  a  characteristic  of  this  accident.  This  is 
accompanied  with  coma  and  vasomotor  and  trophic  disturbances  of 
the  limbs  at  times.  In  less  severe  cases  there  are  disturbances  of  speech, 
tremor,  irregular  jerky  movements  and  a  temporary  paraplegia  with 
involvement  of  the  deep  reflexes. 

Intermittent  Hemiplegia  (hemiplegia  sine  materia).  Not  rarely  there 
occur  attacks  of  hemiplegia  which  last  only  a  few  hours  or  a  day  or  two. 
There  is  often  with  them  mental  confusion  and  aphasia.     These  attacks 


440  DISEASES    OF    THE    NERVOUS    SYSTEM 

are  seen  oftenest  in  cerebral  lues;  occasionally  in  epilepsy  and  migraine; 
and  in  other  conditions  in  which  there  are  arterio-renal  defects.  It  is 
supposed  that  in  some  cases  the  paralysis  is  due  to  a  local  spasm  of  the 
cerebral  blood-vessels  (e.g.,  migraine);  in  other  cases  to  the  temporary 
activity  of  an  obliterating  arteritis  (lues);  or  in  other  cases  to  a  local 
oedema  perhaps  associated  with  a  uraemia  or  other  toxic  irritation. 

Pathology. — The  embolic  plug  cuts  off  the  blood-supply  from  a  certain 
area  of  brain  tissue.  In  twenty-four  hours  this  begins  to  soften.  If 
the  area  is  in  the  cortex  it  becomes  red  (red  softening);  if  in  the  white 
and  less  vascular  part,  it  is  usually  white  with  a  few  red  punctate  spots. 
The  red  softening  gradually  becomes  yellow  (yellow  softening).  The 
dead  tissue  gradually  is  absorbed,  leaving  a  cicatrix  or  cyst.  If  the 
embolus  contains  infective  microbes,  there  may  be  a  local  encephalitis 
and  abscess. 

In  thrombosis  there  are  usually  evidences  of  extensive  atheroma  or 
syphilitic  arteritis.  In  those  instances  in  which  the  thrombosis  is  caused 
by  the  blood  state  and  a  weak  heart,  little  arterial  change  occurs.  Athe- 
roma affects  chiefly  the  internal  carotids  and  the  large  arteries  at  the 
base,  viz.,  the  middle,  anterior,  and  posterior  cerebrals  and  the  basilar 
and  vertebrals.  The  branch  of  the  anterior  cerebral  supplying  the 
caudate  and  part  of  the  lenticular  nucleus  is  called  "the  artery  of  cerebral 
thrombosis." 

Among  seventy-two  cases  of  cerebral  softening  with  autopsy  collected  by  Dr. 
B.  R.  Hoobler  from  hospital  records,  the  site  of  the  lesion  was  as  follows: 


Frontal  lobe 

6 

Parietal  lobe 

17 

Occipital  lobe 

4 

Temporal  lobe 

9 

Caudate  nucleus 

5 

Lenticular  nucleus 

16 

Optic  thalamus 

6 

Internal  capsule 

6 

Corpus  callosum 

2 

Pons  medulla 

1 

72 

This  shows  that  about  half  (35)  involve  the  central  and  half  the 
cortical  arteries.  The  posterior  cerebral  is  involved  in  about  one-third 
of  the  cases.  The  parietal  lobe  and  the  caudate  nucleus  are  most  often 
affected.  Most  of  these  cases  are  thrombotic.  Embolism  almost  always 
affects  the  great  basal  ganglia  or  some  cortical  branch  of  the  anterior 
and  middle  cerebrals. 

The  secondary  changes  after  thrombosis  resemble  those  after  em- 
bolism; a  thrombus,   however,  may  lead  to  supplementary  embolism 


DISEASES    OF   THE   BRAIN  441 

through  breaking  off  of  a  clot,  and  both  conditions  may  cause  a  complicat- 
ing cerebral  hemorrhage. 

The  Diagnosis. — The  important  points  have  been  gone  over  under 
the  head  of  hemorrhage. 

Very  high  blood-pressure,  evidence  of  marked  intra-cranial  pressure, 
very  sudden  onset  with  profound  coma,  respiratory  embarrassment, 
paralysis  and  fatal  termination  point  to  hemorrhage.  Increased  blood- 
pressure  and  temperature  on  the  paralyzed  side  suggest  hemorrhage. 
Lumbar  puncture  and  withdrawal  of  cerebrospinal  fluid  may  give 
definite  eivdence  of  hemorrhage,  but  will  not  exclude  it. 

Premonitory  symptoms  covering  one  or  more  days  indicate  softening. 
A  preceding  period  of  feeling  unusually  well  precedes  some  acute  and  fatal 
hemorrhages. 

Slow  steady  loss  of  consciousness  ending  in  very  deep  coma  indicates 
hemorrhage. 

Recurrent  mild  apoplectic  seizures  are  probably  always  thrombotic. 
Very  slowly  developing  seizures,  coming  on  over  a  period  of  several  days 
are  thrombotic. 

Embolism  is  distinguished  from  thrombosis  by  the  age,  the  presence 
of  endocarditis,  of  the  puerperium  or  septic  fever,  and  by  its  sudden 
onset,  with  perhaps  some  convulsive  movements. 

The  prognosis  as  regards  the  attack  is  somewhat  better  than  in  hemor- 
rhage, as  a  rule.  In  embolism  it  is  good  as  regards  recurrence;  in  throm- 
bosis, bad,  unless  the  trouble  be  due  to  syphilis  or  some  preventable 
cause  like  gas  poisoning.  The  recovery  from  attacks  is  more  complete 
in  acute  softening.  After  the  chronic  stage  is  reached,  however,  the 
prognosis  is  about  the  same  in  all  forms. 

The  treatment  of  the  attacks  consists  essentially  in  rest  and  such 
attention  to  the  bowels,  kidneys,  and  heart  as  may  be  indicated.  In 
thrombosis  it  may  be  important  to  give  heart  stimulants  and  arterial 
depressants,  and  for  this  purpose  I  advise  the  use  of  alcohol  and  of  digi- 
talis, or  strophanthus  with  nitroglycerin.  Thrombosis  is  much  associated 
with  syphilis  and  treatment  must  be  given  accordingly.  It  is  also  often 
associated  with  weakened  and  senile  conditions  and  here  individual 
treatment  involving  tonic  measures,  and  rest  are  indicated.  The 
symptomatic  treatment  of  the  chronic  stage  is  the  same  as  in  hemorrhage. 

SPECIAL  FORMS  OF  HEMORRHAGIC  OR  THROMBOTIC  SOFTENING 

Small  or  large  foci  of  softening  attack  the  brain  in  different  parts 
causing  many  symptom  groups.  A  description  of  these  is  given  under 
the  head  of  softenings,  as  this  is  the  most  frequent  condition. 

Pseudo-bulbar  paralysis  or  cerebral  bulbar  paralysis  is  a  condition 


442  DISEASES    OF    THE    NEKVOUS    SYSTEM 

characterized  by  double  hemiplegia  with  involvement  of  the  bulbar 
centres,  so  that  there  is  difficulty  in  speech,  mastication  and  swallowing. 
It  is  caused  by  a  double  lesion  usually  a  softening  involving  the  motor 
paths  between  the  cortex  and  the  nuclei  in  the  centers  of  the  motor  V 
and  of  the  VII,  IX,  XII  nerves.  Very  rarely  a  one-sided  lesion  may 
cause  this  condition.  The  condition  may  occur  in  the  aged  and  is  then 
due  to  lacunar  degeneration  and  softening. 

As  one  sees  it  in  the  clinic  and  hospital,  pseudo-bulbar  paralysis 
occurs  oftenest  as  the  result  of  a  second  hemiplegic  attack  affecting  the 
sound  side  of  the  brain  in  an  old  hemiplegia.  Occasionally  it  comes  on 
suddenly  and  is  caused  by  acute  bilateral  vascular  lesions.  The  seat  of 
the  lesions  is  usually  in  the  neighborhood  of  the  lenticular  nuclei,  and 
they  are  so  located  that  they  involve  the  fibres  from  the  lower  third  of 
the  motor  cortex  where  the  centres  for  the  throat,  tongue  and  face  lie. 
The  consequence  is  that  there  is  no  great  involvement  of  the  arms  or  legs. 

The  condition  is  a  rare  one.  The  symptoms  are  much  like  those  of 
bulbar  paralysis,  but  the  diagnosis  is  easily  made  by  consideration  of  the 
history,  the  absence  of  muscular  atrophy  and  fibrillary  tremor,  and  the 
marked  involvement  of  the  pyramidal  tracts.  The  disease  tends  to 
improve  rather  than  progress,  as  in  true  bulbar  palsy. 

Thalamus  Apoplexy. — A  hemorrhage  here  causes  usually  a  temporary 
hemiplegia,  with  anaesthesia,  which  latter  symptom  continues.  There 
may  be  later  dysthesise  and  pains  of  the  extremities  and  perhaps  athetoid 
or  choreic  movements.  Sometimes  there  is  hemianopsia;  generally  the 
deep  reflexes  are  not  exaggerated.  A  group  of  symptoms  has  been  noted 
forming  the  thalamic  syndrome.     It  consists  of: 

1.  Hemiansesthesia. 

2.  Hemiataxia. 

3.  Involuntary  and  spontaneous  movements. 

4.  Central  pains. 

5.  Cutaneous  hypersesthesia  of  the  affected  side,  with  overaction  to 
pleasurable  stimuli. 

6.  Hemianopsia;  visual  hallucinations. 

In  some  cases  there  is  paralysis  of  emotional  facial  expression  on  the 
affected  side,  while  voluntary  control  of  the  facial  muscles  is  retained. 

Mid-brain  softenings  are  not  very  rare.  They  are  generally 
luetic  or  arterio-sclerotic.  Hemorrhage  and  tumors  are  less  common. 
Many  different  groups  of  symptoms  may  result.  The  accompanying 
Fig.  213  from  Edinger,  in  connection  with  Fig.  214,  shows  how  the 
different  ''syndromes"  result  in  accordance  with  the  location  of  the 
lesion.     (See  also  Tumors  of  the  Brain.) 

Peduncular  hemiplegia  is  usually  due  to  a  tumor,  but  there  may  be 
a  softening,  from  a  luetic  meningitis  or  thrombosis.     The  lesionhere 


DISEASES    OF    THE   BRAIN 


443 


causes  a  paralysis  of  the  third  nerve  on  the  side  of  the  lesion  and  hemi- 
plegia of  the  opposite  side  (Weber's  syndrome). 

Softening  of  the  Pons. — Softening  in  the  pons  is  most  apt  to  be  in 
the  ventral  part,  near  the  raphe  and  next  to  this  in  the  dorsal  part  of 
the  pons.  The  basilar  artery  or  its  transverse  branches  are  involved. 
Lesions  of  the  pons  alone  are  rarer  than  those  involving  also  the  medulla, 
especially  its  upper  part,  because  the  basilar  is  not  plugged  as  often  as 
the  vertebrals  and  its  branches.  The  prodi'omal  symptoms  are  not 
so  long.  In  a  typical  attack  due  to  plugging  of  the  basilar,  we  get 
a  softening  of  the  deeper  ventral  parts  of  the  pons.  The  patient  suffers 
from  hemiplegia,  with  some  paresis  on  the  opposite  side  to  the  hemi- 


Fig.  213. — ^Lesions  of  the  midbrain  and  resulting  symptoms.  2.  Hemianopsia; 
3.  disturbances  of  pupillary  light-reflex;  4.  ipso-lateral  paralysis  of  eye-muscles, 
contra-lateral  hemiansesthesia,  forced  movements,  tremors;  5,  as  in  4  plus  crossed 
hemiplegia;  6,  crossed  motor  and  sensory  disturbance  with  slight  oculo-motor  symp- 
toms on  same  side;  7,  one-sided  or  double-sided  oculo-motor  paralysis,  complete  dila- 
tation of  pupils,  amblyopia;  1.8,  hemiansesthesia,  central  pain,  visual  hallucinations. 

plegia.  There  is  great  exaggeration  of  reflexes  and  twitching  spasms 
and  coarse,  irregular,  jerky  movements  of  the  limbs,  but  no  convul- 
sion. There  is  usually  anaesthesia  and  ataxia  on  the  side  of  the  lesion, 
and  the  anaesthesia  is  dissociated.  There  is  often  forced  weeping  and 
laughter  and  dysarthria  may  occur.  Forced  movements  are  not  common. 
When  the  lesion  is  high  up  and  involves  some  of  the  transverse  branches 
of  the  basilar,  we  get  oculo-motor  palsies  and  spasmodic  disorders  on 
the  side  of  the  lesion  and  paralysis  and  anaesthesias  on  the  opposite  side. 
When  lower  down,  we  get  fifth  and  seventh  nerve  palsies  on  one  side  and 
hemiplegia  on  the  other.  ^  In  basilar  artery  lesion,  if  the  injury  is  large  and 
severe,  the    patient  develops  disorders  of   deglutition  and   speech  and 

^Foville's  Paralysis. — A  "crossed  hemiplegia"  with  paralysis  of  the  sixth  and 
seventh  nerves  on  the  side  of  the  lesion  and  paralysis  of  the  extremities  on  the 
opposite  side. 


444 


DISEASES    OF    THE    NERVOUS    SYSTEM 


extension  of  the  process  and  dies  from  paralysis  of  the  bulbar  centres. 
No  great  disturbances  of  temperature  occur,  nor  are  there  marked 
pupillary  symptoms.  In  the  smaller  lesions  due  to  involvement  of  the 
transverse  branches  recovery  may  occur,  leaving  the  patient  with  a 
crossed  paralysis. 


Mid-brain,  t'  1 


To  cerebellum. 


To  cerebellum. 


Medulla. 


Cord. 


Direct  cerebellar  tract. 

Spino-cerebellar  (Gower's  tract). 

Temperature  and  pain  tract. 

Tactile. 

Tactile. 

Muscle  sense. 


Fig.  214. — Showing  how  le,sion8  in  medulla  and  pons  may  cause  focal  symptoms  by 
cutting  off  tracts  and  destroying  cranial  nerve  nuclei.  The  motor  tracts  lie  deep  be- 
low the  sensory  and  begin  to  cross  in  the  lower  medulla  and  cord.  They  are  not 
indicated  here. 


When  the  lesion  is  such  as  to  cause  paralysis  of  the  facial  nerve  on 
the  side  of  the  lesion  and  hemiplegia  on  the  opposite  side,  we  have  what 
is  called  the  Millard-Gubler  syndrome. 

Softening  of  the  Medulla.- — Softening  is  rare,  but  much  more  frequent 
than  hemorrhage.  It  occurs  at  the  early  apoplectic  age — thirty  to  fifty, 
oftener  in  males,  and  is  due  to  lues  and  the  arterial  changes  associated 


DISEASES    OF    THE    BRAIN  445 

with  alcoholism  and  nephritis.  It  has  been  observed  as  a  result  of  work- 
ing in  compressed  air. 

A  small  lesion  may  cause  tetraplegia;  or  it  may  be  low  down  involving 
the  leg  fibres  of  the  pyramidal  tract  after  they  have  crossed  and  the  arm 
fibres  before  they  have  crossed.  This  causes  paralysis  of  the  arm  on  the 
contralateral  side,  of  the  leg  on  the  homo-lateral  side  (hemiplegia 
cruciata).^ 

A  rather  special  syndrome  is  caused  by  thrombosis  of  the  inferior 
cerebellar  artery.  The  symptoms  may  come  on  slowly  almost  like  a 
tumor.  Finally  a  seizure  occurs  with  symptoms  which  vary  somewhat, 
but  are  about  as  in  the  following  table: 

Homolateral  side  Contralateral  side 


Paralysis  Hemiplegia. 

of  soft  palate  Cutaneous     anaesthesia     for     pain     and 

of  vocal  cord  temperature 

of  Trigeminus 

of  facial 

of  sympathetic 
Cerebellar  ataxia  +  +  +  I  Ataxia  ? 


The  cause  of  the  symptoms  is  shown  in  Fig.  214.  The  tracts  for  muscular 
and  tactile  sensations  have  not  altogether  crossed  in  the  medulla,  hence 
we  may  get  some  evidence  of  ataxia  on  both  sides.  But  the  cerebellar 
tracts  and  peduncle  injured  have  not  crossed. 

CHRONIC  PROGRESSIVE  SOFTENING  OF  THE  BRAIN 

Sometimes  thrombotic  processes  affect  especially  and  successively 
the  smaller  central  arteries  of  the  circle  of  Willis  and  lead  to  a  gradual 
softening.  With  this  process  there  develops  a  gradual  hemiplegia 
coming  on  perhaps  in  stages  during  the  course  of  six  months  or  a  year. 
With  the  hemiplegia  there  may  be  headaches,  vertigo,  paresthesia  and 
anaesthesia,  dysarthria  with  some  mental  deterioration.  The  pro- 
gressive character  of  the  disease  suggests  a  brain  tumor  or  abscess. 
In  very  severe  cases  there  may  be  optic  neuritis  and  atrophy.  Usually, 
after  reaching  a  certain  stage,  the  disease  is  arrested  and  the  patient 
remains  about  the  same  for  some  years. 

^  Hughlings- Jackson's  syndrome  is  a  condition  produced  by  medullary  lesions  in 
which  there  is  hemi-atrophy  of  the  tongue  and  paralysis  of  the  trapezius,  sterno- 
mastoid,  vocal  cord  and  soft  palate,  all  on  the  same  side. 


446  DISEASES    OF    THE    NERVOUS    SYSTEM 

Senile  hemiplegia.- — -Marie  has  described  a  condition  known  as 
lacunar  degeneration.  It  is  characterized  by  the  presence  of  cavities  of 
various  sizes  (J^f  o  to  ^^  inch)  and  irregular  contour  distributed  through 
the  brain.  Through  these  cavities  runs  a  sclerotic  but  permeable 
blood-vessel.  The  softening  is  not  thrombotic  but  due  to  the  disease 
of  the  vessel  wall  and  interference  with  the  nutrition  by  the  ordinary 
peri-vascular  exchanges.  The  presence  of  lacunar  degeneration  leads  to 
attacks  of  hemiplegia  which  are  usually  mild  and  sometimes  temporary. 
They  may  not  be  accompanied  with  loss  of  consciousness  or  abolition  of 
the  skin  reflexes.  Lacunar  degeneration  thus  causes  a  hemiplegia  of 
the  aged. 

Lacunar  degeneration,  associated  with  arterial  sclerosis  is  one  of  the 
factors  in  chronic  senile  paraplegia,  characterized  by  short-step  gait 
{demanche  a  petit  pas). 

THROMBOSIS  OF  THE  CEREBRAL  SINUSES 

Sinus  thrombosis  may  be  non-inflammatory  or  inflammatory.  Non- 
inflammatory thrombosis  is  due  to  a  weak  heart  and  usually  occurs 
in  children  under  the  age  of  one  year,  in  very  old  people,  or  at  the  end  of 
exhausting  diseases. 

Inflammatory  sinus  thrombosis  is  due  to  some  neighboring  bone 
disease,  especially  otitic  disease.  However,  any  disease  of  the  bones  of 
the  skull  and  especially  of  the  orbital  and  nasal  cavities,  may  give  rise  to 
the  thrombosis  as  nearly  all  the  sinuses  receive  a  small  venous  supply 
from  the  exterior  of  the  skull. 

Sinus  thrombosis  from  exhausted  conditions  and  weak  heart  affects 
usually  the  longitudinal  sinus.  Otitic  thrombosis  affects  the  lateral 
(transverse)  superior  and  inferior  petrosal  sinuses.  Orbital  thrombosis 
affects  especially  the  cavernous  sinus. 

The  general  symptoms  of  sinus  thrombosis  vary  greatly  according  to 
the  part  affected,  the  extent  of  the  obstruction,  the  primary  cause,  and 
the  complications.  There  are,  therefore,  symptoms  of  cardiac  weakness 
and  marasmus,  or  of  otitic,  orbital,  nasal  or  other  cranial  bone  disease,  with 
corresponding  local  and  general  symptoms  of  infection. 

The  cerebral  symptoms  vary  also  but  resemble  those  of  an  acute 
meningitis,  or  of  a  focal  hemorrhage  or  softening.  There  occur  head- 
ache, vomiting,  stiff  neck,  delirium,  coma,  convulsions,  hemiplegia,  apha- 
sia.    There  is  rarely  temperature  from  the  thrombosis  alone. 

Some  of  the  special  sinus  symptoms  are  as  follows: 

In  cavernous  sinus  thrombosis,  there  are  dilated  facial  veins,  pro- 
trusion of  the  eyeballs  with  orbital  oedema,  due  to  swelling  of  the  retro- 
bulbar veins,  sometimes  choked  disc,  supra-orbital  pain  and  involvement 
of  the  motor  nerves  of  the  eye  (Fig.  215). 


DISEASES    OF    THE   BRAIN 


447 


In  thrombosis  of  the  lateral  (transverse)  sinus,  there  is  swelling 
and  oedema  over  and  about  the  mastoid,  with  tenderness  in  this  region 
and  along  the  jugular  vein,  in  which  a  clot  may  be  felt.  There  is  pain 
locally  and  on  lateral  movement  of  the  head,  and  on  swallowing.  If 
the  thrombosis  is  not  septic  or  complete  and  solid  the  subjective  symptoms 
may  be  slight. 

If  it  is  a  septic  thrombosis  there  are  symptoms  of  general  infection, 
and  of  cerebral  involvement.  These  latter  most  often  resemble  those 
of  meningitis,  though  lumbar  puncture  will  not  show  lymphocytosis. 


Fig.  215. — Exophthalmus,  thrombosis  of  cavernous  sinus. 
{Weldebrandt  and  Sanger.) 

In  thrombosis  of  the  longitudinal  sinus  there  is  swelling  especially 
of  the  frontal  and  parietal  veins,  causing  the  caput  Medusce;  sometimes 
nose-bleed,  and  in  infants  distended  fontanelles. 

The  prognosis  in  primary  thrombosis  is  not  good,  but  cases  may 
recover.  In  infective  thrombosis,  the  prognosis  is  very  serious  unless 
there  can  be  surgical  interference. 

The  treatment  of  sinus  thrombosis  is  symptomatic  and  surgical. 
Its  details  are  largely  in  the  hands  of  otologists,  rhinologists  and  general 
surgeons. 


CEREBRAL  PALSIES  OF  CHILDREN— INFANTILE  HEMIPLEGIA  AND 

DIPLEGIA 

The  brain  palsies  of  early  life  show  themselves  in  the  form  of  (1) 
hemiplegias;  (2)  diplegias  or  double  hemiplegias,  in  which  both  sides 
of  the  body  are  involved;  and  (3)  paraplegias,  in  which  the  lower  limbs 


448  DISEASES    OF    THE    NERVOUS    SYSTEM 

are  chiefly  or  entirely  involved.  In  these  palsies,  as  in  the  same  troubles 
of  adult  life,  the  loss  of  motor  power  is  always  accompanied  by  a  rigidity 
and  by  some  contractures  and  exaggeration  of  reflexes,  in  this  respect 
distinguishing  these  paralyses  from  those  of  spinal  origin.  The  seat  of 
lesion  in  these  cases  is  in  the  hemispheres  of  the  brain,  and  it  is  the 
upper  motor  neurons  which  are  involved;  that  is  to  say,  that  part  of  the 
direct  motor  tract  which  extends  from  the  brain  cortex  down  to  the  spinal 
cord  as  far  as  the  anterior  horns.  The  brain  palsies  of  children  are  there- 
fore disorders  of  the  cortico-spinal  neurons,  while  the  spinal  palsies  of 
children  are  disorders  of  the  lower  neurons. 

I  have  reserved  the  term  Little's  disease  for  those  cases  of  cerebral 
diplegia  due  to  agenesis  of  the  pyramidal  tracts. 

Etiology.- — The  disease  occurs  rather  oftener  in  males  than  in  females, 
though  the  difference  is  slight.  The  vast  majority  occur  in  the  first 
three  years  of  life;  about  one-third  of  them  are  congenital.  Injuries 
to  the  mother  during  the  time  of  pregnancy,  possibly  diseases  and  emo- 
tional disturbances  at  this  time,  are  factors  in  producing  the  congenital 
cases.  Those  cases  that  occur  at  the  time  of  birth  are  due  to  tedious 
labor,  the  use  of  forceps,  and  other  injuries  at  the  time  of  parturition. 
After  birth,  the  causes  are  those  which  lead  to  the  production  of  intra- 
cranial hemorrhages,  embolism,  and  thrombosis;  these  being  injuries 
and  the  infectious  fevers.  Of  the  latter,  pneumonia,  encephalitis,  whoop- 
ing-cough, measles,  and  scarlet  fever  are  the  most  prominent.  Syphilis 
is  a  cause  in  15  to  20  per  cent.;  cerebrospinal  meningitis  and  epileptic 
convulsions  are  also  occasional  causes. 

Symptomatology. — The  disorder  in  about  one-fourth  of  the  cases 
begins  with  a  convulsion,  which  may  be  unilateral,  but  is  usually  general 
in  character,  and  may  last  for  several  hours.  At  the  same  time  a  febrile 
process  develops,  and  this  continues  for  several  days.  When  these  acute 
symptoms  have  subsided,  or  before  this,  it  is  noticed  that  the  child  is 
paralyzed  upon  one  side,  the  paralysis  involving  the  arm,  leg,  and  face, 
as  in  adult  hemiplegia,  or  perhaps  involving  both  sides.  This  paralysis 
undergoes  gradual  improvement,  the  face  recovering  earliest  and  most, 
the  leg  next,  and  the  arm  least.  As  the  child  develops  it  is  found  that 
the  paralyzed  side  fails  to  grow  as  fast  as  the  other,  and  there  may  be 
from  one-half  to  one  inch  or  two  inches  of  shortening  in  the  arm  or  leg. 
The  circumference  of  the  limbs  is  less,  the  surface  somewhat  colder,  and 
some  vasomotor  disturbance  may  be  present.  With  the  progress  of  the 
case  a  rigidity  of  the  affected  limbs  develops;  the  heel  becomes  drawn  up, 
so  that  there  is  talipes  equino-varus  or  equino-valgus.  The  flexors  of 
the  forearm  and  of  the  wrist  and  fingers  contract,  as  do  also  the  adductors 
of  the  thighs.  In  general  it  will  be  found  that  there  is  a  contraction  of  the 
flexors  and  adductors  of  the  affected  limbs.     With  this  rigidity  and  the 


DISEASES    OF   THE   BEAIN  449 

contractures  there  are  exaggeration  of  reflexes  and  clonus  in  most  cases. 
In  the  disordered  Hmbs  pecuHar  mobile  spasms  develop.  These  consist 
of  athetoid,  choreic,  and  ataxic  movements,  also  sometimes  tremors  and 
associated  movements.  The  choreic  and  athetoid  movements  are  the 
most  common. 

Along  with  the  appearance  of  these  symptoms  it  is  noticed  that  there 
are  disturbances  in  the  mental  condition  of  the  child.  It  is  usually  back- 
ward in  development,  this  backwardness  ranging  from  simply  feeble- 
mindedness to  complete  idiocy.  Taking  all  cases,  there  is  about  an  equal 
division  between  feeble-mindedness,  imbecility,  and  idiocy  (Sachs). 
Perhaps  a  little  over  one-fourth  of  the  subjects  have  a  fair  intelligence. 
There  is  usually  slowness  in  learning  to  talk,  and  in  a  small  proportion  of 
cases  there  is  a  decided  aphasia.  Such  condition  is  rather  more  frequent 
with  right  hemiplegia  than  with  left  hemiplegia,  though  the  rule  is  not  an 
absolute  one.  In  connection  with  the  mental  defect  there  may  develop 
many  of  the  peculiar  moral  traits  associated  with  idiocy  and  low  degrees 
of  intelligence.  Epilepsy  very  frequently  complicates  the  disease;  nearly 
one-half  of  the  subjects  suffer  from  this  trouble.  This  epilepsy  is  in 
most  cases  general  in  character;  in  a  few  cases  it  takes  the  Jacksonian 
type,  in  a  small  number  petit  mal  alone  is  noted.  Examination  of  this 
class  of  sufferers  reveals,  aside  from  the  paralysis  described,  various  evi- 
dences of  defective  development.  These  are  known  as  stigmata  of  de- 
generation; though  they  cannot  be  classed  strictly  among  such,  since 
they  are  acquired  stigmata  in  most  cases,  rather  than  marks  which  are 
the  result  of  primary  deficiency  in  development.  These  stigmata  con- 
sist of  a  microcephalic  or  a  macrocephalic  skull,  cranial  and  facial  asym- 
metry, prognathism,  imperfectly  developed  teeth,  and  a  high  palatal 
arch.  It  has  been  found  that,  as  a  rule,  in  cases  of  cerebral  hemiplegias  of 
childhood  the  patient  eventually  has  a  slight  flattening  of  the  skull  on 
the  side  of  the  lesion  (Fisher  and  Peterson) .  Finally,  in  a  few  cases  there 
may  be  found  defects  in  the  special  senses,  such  as  imperfect  hearing, 
deafness,  deaf-mutism,  and  defects  in  vision,  such  as  hemianopsia,  and 
perhaps  imperfections  in  smell  and  taste.     Anaesthesia  is  never  observed. 

The  symptoms  in  the  cerebral  palsies  of  children,  having  passed  the 
acute  stage  and  having  become  somewhat  ameliorated,  enter  into  a 
chronic  stage.  This  chronic  stage  begins  within  a  few  months  after 
birth  or  after  the  onset  of  the  disease.  No  great  change  occurs  in  the 
paralyses  as  the  child  grows  older  until  he  reaches  the  time  of  puberty, 
though  there  is  a  slight  improvement  in  most  cases.  After  the  time  of 
puberty,  if  the  mental  condition  of  the  child  is  good,  the  physical  symp- 
toms are  apt  to  improve  considerably. 

Morbid  Anatomy .^ — The  primary  changes  that  lead  to  the  cerebral 
palsies  of  children  are:  1st,  simple  agenesis  or  lack  of  brain  development, 

29 


450 


DISEASES    OF   THE    NERVOUS    SYSTEM 


producing  localized  atrophy  of  the  cerebrum  and  the  condition  known  as 
porencephalus,  a  condition  in  which,  owing  to  a  congenital  defect  in  nutri- 
tion, a  cavity  or  depression  exists  in  the  cerebral  hemispheres,  this  cavity 
reaching  generally  into  the  lateral  ventricle.  True  porencephalus  is 
found  in  about  one-fourth  of  the  cases,  though  no  definite  statistics  can 
be  given,  owing  to  the  different  interpretations  given  to  this  term;  2d, 
hemorrhage,  which  is  probably  the  most  frequent  of  the  single  causes; 
3d,  embolism;  4th,  thrombosis;  5th,  meningo-encephalitis  and  polio- 
encephalitis; 6th,  a  diffuse  cortical  sclerosis.  Many  other  terms  are 
used  to  describe  the  pathological  conditions  found  at  the  basis  of  the 


Fig.  216. — Atrophied  brain  with  sclerosis  and  a  cyst,  from  a  case  of  infantile 
cerebral  hemiplegia. 


brain  palsies  of  children,  but  the  principal  causes  of  all  are  undoubtedly, 
as  has  been  described,  hemorrhages,  encephalitis  and  softenings,  and  a 
defective  development  or  agenesis.  It  is  probable  that  in  the  hemi- 
plegics  the  original  lesion  is  generally  a  central  hemorrhage,  less  often 
a  meningeal  hemorrhage.  After  this,  probably  the  most  frequent  con- 
dition is  a  porencephalus  from  some  intra-uterine  accident,  which  may 
have  been  defective  nutrition  causing  anaemia  and  softening,  or  hemor- 
rhage, or  thrombosis.  Acute  encephalitis  or  inflammation  of  the  brain 
of  the  kind  similar  to  poliomyelitis  is  a  frequent  cause.  In  double 
hemiplegias  or  diplegias  of  children  the  cause  is  in  the  vast  majority  of 
cases  a  hemorrhage  due  to  some  injury  or  disturbance  at  the  time  of  labor. 


DISEASES    OF    THE   BRAIN 


451 


In  other  cases  of  diplegia  the  lesion  isadoubleporencephalus,  which  maybe 
either  the  result  of  an  intra-uterine  hemorrhage  or  simply  a  defective  de- 
velopment. In  the  paraplegias  the  lesion  is  probably  very  much  the  same  as 
in  the  diplegias,  that  is  to  say,  either  a  meningeal  hemorrhage  or  a  brain 
agenesis.  Occasionally  a  diffuse  sclerosis  has  been  found  in  these  cases. 
Not  infrequently,  as  the  result  of  hemorrhages,  there  develop  cysts  which 
fill  up  the  atrophied  areas  of  the  brain  (Fig.  216).  It  is  difficult  to  pre- 
sent accurately  and  definitely  the  relations  between  the  pathological 
change  and  the  clinical  result,  but  it  may  be  shown  with  some  degree  of 
correctness  in  the  following  table. 


Original  Lesions 

Later  Pathological  Conditions                          Clinical  Result 

Hemorrhage. 

Atrophy. 

Hemiplegia. 

Embolism. 

Lobar  and  diffuse  sclerosis. 

Diplegia. 

Thrombosis. 

Cysts. 

Paraplegia. 

Agenesis. 

Porencephaly. 

Sensory  defects. 

Encephalitis. 

Microcephaly. 

Mental  defects. 
Epilepsy,  etc. 

Diplegia  or  Birth  Palsies. — That  form  of  the  brain  palsies  of  childhood  character- 
ized by  double  hemiplegias  or  diplegias  has  certain  special  characters  which  lead  to 
its  being  often  classed  apart.  These  diplegias  in  almost  all  cases  are  congenital  and 
are  due  either  to  injuries  at  the  time  of  birth  or  to  some  disorders  of  intra-uterine  life. 
There  may  be  convulsions  or  a  prolonged  state  of  asphyxia  at  the  time  of  birth.  After 
recovery  from  this  no  special  trouble  is  noticed  with  the  child  by  the  mother  for  some 
weeks  or  months,  when  it  will  be  found  that  it  does  not  use  its  arms  or  legs.  Other 
convulsions  develop,  and  eventually  the  features  of  a  double  hemiplegia  with  mental 
impairment  and  epilepsj^  are  observed.  In  these  cases  the  mental  defect  is  much 
more  decided  than  in  the  hemiplegias;  indeed,  few  of  these  cases  ever  show  any  good 
amount  of  intelligence.  Epilepsy  is  extremely  common.  The  anatomical  lesion 
in  the  cases  is,  as  already  stated,  either  a  meningeal  hemorrhage  which  has  pressed 
upon  and  injured  the  cortical  motor  areas  in  each  hemisphere,  or  it  is  a  congenital 
porencephalic  defect.     (See  Little's  Disease.) 

Diagnosis. — The  clinical  diagnosis  of  cerebral  palsies  is  to  be  made 
from  the  spinal  palsies.  The  latter  are  distinguished  by  the  fact  that  in 
the  infantile  paralyses  of  spinal  origin  there  is  no  rigidity  or  exaggeration 
of  reflexes,  and  there  are  electrical  degenerative  reactions  of  the  muscles 
and  decided  wasting  of  the  limbs  with  shortening.  The  mode  of  onset  in 
cerebral  palsies  and  their  distribution  in  the  form  of  hemiplegias  in  which 
the  face  is  involved  also  indicate  the  seat  of  the  lesion.  The  pathological 
diagnosis  is  by  no  means  an  easy  one.  Cerebral  palsies  occurring  at  the 
time  of  birth  and  accompanied  at  the  time  by  general  convulsions  or 
asphyxia  may  be  considered  to  be  due  to  meningeal  hemorrhage,  espe- 
cially if  the  delivery  of  the  child  has  been  brought  about  by  the  use  of 


452  DISEASES    OF    THE    NERVOUS    SYSTEM 

forceps  or  if  the  labor  has  been  long  and  tedious.  Diplegias  and  para- 
plegias which  are  congenital  are  probably  due  to  true  porencephalus,  pro- 
vided there  was  no  difficulty  at  the  time  of  labor  and  there  were  no  con- 
vulsions or  other  serious  phenomena  after  it.  Cerebral  palsies  occurring 
after  birth  in  the  first,  second,  or  third  year  of  life  are  apt  to  be  due  to 
hemorrhage  and  encephalitis,  less  often  to  embolism  or  thrombosis. 
Hemiplegias  developing  after  infectious  fevers  are  likely  to  be  due  to 
hemorrhage.  In  diagnosticating  the  pathological  lesion  in  such  cases  it 
must  always  be  remembered  that  hemorrhage  is  much  more  frequent 
than  embolism,  and  that  thrombosis  occurs  only  in  children  with  very 
weak  hearts  and  in  marasmus. 

Course  and  Prognosis. — In  all  types  of  the  disease  the  course  is  chronic 
and  perfect  cure  is  hardly  possible,  although  in  the  slighter  forms  of 
hemiplegia  nearly  all  traces  of  the  paralysis  may  be  absent.  In  the  hemi- 
plegic  form  the  patient  often  reaches  adult  life,  and  if  his  intelligence  is 
not  defective  and  he  has  no  epilepsy  the  motor  trouble  improves  a  great 
deal  and  he  may  live  a  long  and  useful  life.  If  epilepsy  and  mental  defect 
are  present,  there  ensues  eventually  a  further  mental  deterioration,  and 
such  subjects  rarely  live  much  beyond  the  period  of  adolescence,  or  if 
they  do  they  pass  into  the  asylums  for  the  idiotic  and  epileptic.  The 
diplegic  and  paraplegic  cases  have  a  much  worse  prognosis  both  as  to 
duration  of  life  and  as  to  improvement  in  symptoms,  except  occasionally 
the  type  described  above  as  due  to  agenesis  of  the  pyramidal  tracts. 
The  degree  of  intelligence  and  the  absence  of  epilepsy  are  the  two  factors 
which  measure  the  seriousness  of  these  cases,  as  they  do  those  of  the  hemi- 
plegias. As  regards  the  significance  of  individual  symptoms,  the  post- 
hemiplegic movements  have  a  bad  import;  the  presence  of  a  microcephalic 
head  or  of  decided  marks  of  degeneration  is  unfavorable. 

Treatment. — The  treatment,  so  far  as  the  paralysis  is  concerned,  is 
largely  mechanical.  The  patient  is  benefited  by  occasional  courses  of 
electrical  treatment  which  stimulate  somewhat  the  nutrition  and  func- 
tions of  the  muscles.  Massage  and  stretching  of  the  contractured  tendons 
and  limbs  also  are  helpful  in  my  experience.  The  orthopaedic  surgeon 
is  able  to  render  valuable  assistance  by  occasional  overstretching  the  con- 
tractured limbs  and  placing  them  in  spUnts.  Tenotomy  may  also  be  re- 
sorted to  with  advantage,  as  I  have  had  occasion  to  see.  The  child 
should  be  encouraged  above  all,  however,  to  use  the  limb  as  much  as 
possible.  He  should  be  taught  gymnastic  exercises;  running,  walking, 
and  bicycle  riding  are  all  measures  which  give  great  help.  When  the 
child's  intelligence  is  good  and  there  is  little  or  no  epilepsy,  a  great  deal 
can  be  expected  in  the  way  of  improvement  as  he  grows  older. 

So  far  as  the  epilepsy  is  concerned,  it  should  be  treated  on  the  same 
principles  as  idiopathic  epilepsy,  except  that  great  care  should  be  had  in 


DISEASES    OF   THE   BRAIN  453 

the  use  of  the  bromides;  a  thorough  test  must  be  made  in  order  to  de- 
termine how  much  of  this  drug  will  suppress  the  fits,  and  then  its  use 
must  be  graduated  in  the  future  in  accordance  with  the  knowledge  thus 
obtained.  The  mental  defects  of  the  child  can  be  helped  only  by  proper 
training  of  the  body  and  careful  education  of  the  mind.  The  question 
of  operative  interference  in  these  cases  has  excited  much  attention.  A 
priori  it  would  not  seem  as  though  surgical  interference  could  do  good  in 
relieving  conditions  in  which  there  is  destroyed  or  atrophic  tissue.  Still 
the  subject  must  be  dealt  with  empirically,  and  there  have  been  some 
results  which  show  that  apparently  a  relief  is  obtained  in  a  few  cases  by 
trephining  the  skull  and  if  he  then  finds  any  evidences  of  compression 
from  the  presence  of  a  cyst,  this  may  be  very  cautiously  opened.  Resec- 
tion of  the  posterior  spinal  roots  has  been  tried  with  some  successes 
reported. 


CHAPTER  XIX 
TUMORS  OF  THE  BRAIN 

All  forms  of  new  growths  are  found  in  the  brain,  but  the  infectious 
granulomata,  tubercle  and  gumma,  and  the  sarcomatous  type  of  tumors 
are  the  most  common.  Gushing  found  that  64  per  cent,  of  brain  tumors 
were  gliomata  and  gliomatous.  Elsberg's  statistics  show  about  the 
same  proportion.^ 

^  In  order  to  present  a  working  view  of  brain  tumors  from  a  surgical  standpoint, 
Dr.  Charles  A.  Elsberg  has  kindly  furnished  me  an  analysis  of  100  cases  subjected 
to  radical,  exploratory  or  palliative  operation.  The  figures  naturally  are  not  the 
same  as  those  derived  from  a  series  of  post-mortem  studies  like  those  of  Schlessinger. 
but  they  represent  more  accurately  the  kind  of  cases  that  come  to  the  neurologist, 
I  present  only  the  salient  features  of  his  analysis. 

Location 

Cerebral  44 

Cerebellar  or  pontine  28 

Unlocalized  20 

Cortical  or  extra-cortical  14 

Deeply  subcortical  68 

Not  locahzed  28 

Frontal,  central  and  parietal  21 

Occipital  and  temporal  5 

Thalamic,  3d  ventricle  and  mid-brain  10 

Hypophysis  and  peduncular  region  8 

Cerebellum  20 

Cerebello-pontine  angle  7 

Pontine  1 

Nature  of  Growth 

GHoma  33 

Gliomatous  cyst  3 

Gliosarcoma  1 

Sarcoma  3 

Endothelioma  5 

Adenoma  5 

Teratoma                              ,  1 

Cholesteatoma  1 

Neurofibroma  5 

Simple  cyst  2 

Nature  unknown  (no  examination)  13 

Nature  unknown  (unlocalized)  28 

100 
Operative  Result 

Tumor  was  removable  and  removed  in  13 

Tumor  was  partly  removed  in  5 

Cyst  (non-gliomatous)  was  evacuated  in  2 
Tumor  could  not  be  removed  on  account  of 
nature  or  location,  or  the  tumor  was  not 

localized  in  80 


100 


454 


TUMORS    OF    THE   BRAIN  455 

Etiology. — Brain  tumors  affect  males  oftener  than  females,  the  ratio 
being  about  as  two  to  one  (644  :320).  Sarcomata  alone  seem  to  affect 
females  about  as  often  as  males.  Brain  tumors  occur  with  about  equal 
frequency  throughout  all  ages  of  life  up  to  about  fifty;  one-third  occur 
under  the  age  of  twenty  (Gowers).  During  childhood  tumors  are  about 
equally  distributed  throughout  all  ages  (Starr).  One-half  of  all  the 
tumors  of  childhood  are  tuberculous;  after  this  come  gliomata,  endo- 
theUomata  and  sarcomata.  The  gumma,  ghoma  and  sarcoma  begin  to 
be  more  frequent  after  the  age  of  twenty.  Sarcoma  and  especially  cancer 
occur  in  the  middle  and  later  ages  of  hfe;  but  brain  tumors  of  any  kind 
are  extremely  rare  after  the  age  of  sixty. 

To  sum  up  in  tabular  form,  the  relative  frequency  of  the  different 
kinds  of  tumors  with  regard  to  age  is  shown  in  the  following : 

Childhood,  tubercle,  parasites. 

Early  life,  gumma,  glioma,  parasites. 

Early  and  middle  life,  sarcoma,  endotheUoma,  glioma,  and  gumma. 

Middle  and  late  life,  sarcoma,  endothelioma,  gumma,  cancer. 

Heredity  has  a  shght  influence  in  predisposing  to  brain  tumors. 
Blows  on  the  head  and  other  forms  of  injury  to  the  cranium  are  exciting 
causes  in  a  small  proportion  of  cases.  Practically  all  cancers  and  many 
sarcomata  of  the  brain  are  metastatic  in  origin. 

Seat. — About  one-fourth  of  all  tumors  are  in  the  cerebellum,  or  cere- 
bello-pontine  angle,  and  about  one-fourth  are  in  the  frontal  lobe.  About 
one-twelfth  of  all  tumors  are  in  the  basal  ganglia  and  lateral  ventricles, 
and  a  rather  smaller  number  in  the  mid-brain  and  medulla.  Tumors  more 
often  lie  in  the  cortex  and  parts  just  below,  than  in  the  centrum  ovale. 

In  children  the  locations  are  a  little  different.  Here  nearly  one-half 
of  the  tumors  are  in  the  cerebellum  and  pons.  They  are  very  much  less 
frequent  in  the  cortex  cerebri  but  more  common  in  the  centrum  ovale, 
basal  ganglia  and  mid-brain.  As  the  mid-brain  as  well  as  all  the  contents 
of  the  posterior  fossa  are  nourished  by  the  vertebral  arteries  and  their 
branches,  it  follows  that  the  majority  of  tumors  in  children  are  in  this 
vascular  area. 

Symptoms. — The  symptoms  of  brain  tumors  vary  extremely  in  ac- 
cordance with  the  location,  the  kind  of  tumor,  the  rapidity  of  growth, 
and  the  age  of  the  patient.  The  general  course  of  a  case  of  brain  tumor 
in  an  adult  is  somewhat  as  follows:  The  patient  first  notices  a  headache 
which  is  intense  and  persistent,  and  which  has  exacerbations  of  frightful 
severity.  With  the  headache  or  between  the  attacks  vomiting  occurs, 
which  is  often  not  accompanied  by  any  nausea.  Sensations  of  vertigo, 
annoying  parsesthesias,  and  convulsive  movements  affecting  one  or  more 

This  indicates  that  about  20  per  cent,  of  brain  tumors  brought  to  a  special  hospital 
or  neurological  surgeon  are  operable. 


456  DISEASES    OF    THE    NERVOUS    SYSTEM 

extremities  develop,  and  there  may  even  be  general  convulsions.  Papill- 
oedema  and  optic  neuritis  may  then  appear  and  the  patient  finds  that  his 
eyesight  is  weak  and  progressively  deteriorating.  The  mind  becomes 
more  or  less  disturbed,  the  mental  processes  are  dull  and  slow,  a  feeling 
of  hebetude  and  incapacity  to  attempt  any  mental  exertion  are  present. 
As  the  disease  progresses  the  intense  pains  and  vomiting  produce  weak- 
ness and  emaciation.  Paralyses  of  various  kinds  develop  and  blindness 
ensues.  Convulsions  of  a  local  or  general  character  become  more  fre- 
quent, and  finally  the  patient  becomes  bed-ridden  and  helpless. 

The  course  of  the  disease  is  not  a  steady  one,  there  being  often  slight 
remissions,  or  there  may  be  periods  when  progress  seems  to  be  arrested. 
After  a  period  of  time  varying  from  one  to  four  or  five  years  death  occurs 
from  exhaustion  or  some  intercurrent  malady. 

The  symptoms  thus  very  briefly  outlined  are  divided  into  general 
and  focal.     The  general  symptoms  are: 

Headache. 

Vertigo. 

Vomiting. 

Papilloedema.  , 

Mental  defects. 

Besides  these  there  may  be  general  convulsions  and  speech  disturb- 
ances. 

Headache  occurs  in  from  one-half  to  two-thirds  of  the  cases;  it  is  very 
severe  and  the  pains  are  of  a  boring  or  lancinating  character;  they  are  so 
horrible  that  they  often  lead  the  patient  to  think  of  suicide.  The  pains 
are  sometimes  periodical,  occurring  every  night  or  every  other  day,  and 
suggest  by  their  periodicity  a  malarial  character.  They  are  located  some- 
times in  the  brow  or  in  the  occiput,  while  sometimes  they  are  diffused 
all  over  the  head;  they  are  rather  more  frequent  than  otherwise  in  the 
neighborhood  of  the  tumor.  They  are  more  frequent  with  cerebellar 
tumors  than  with  those  located  anywhere  else.  They  are  less  frequent 
with  tumors  situated  in  the  peduncles  and  at  the  base  of  the  brain.  The 
pains  are  due  to  the  increased  intra-cranial  pressure  and  to  irritation  and 
stretching  of  the  dura  mater  by  the  encroachments  of  the  new  growth. 
Headache  occurs  in  about  the  same  proportion  in  children  and  adults,  and 
it  does  not  seem  to  bear  much  relation  to  the  kind  of  tumor,  although  the 
pains  are  generally  less  with  the  gliomata,  and  they  are  more  frequent 
with  rapidly  growing  tumors  whatever  their  character.  With  the  pains 
there  is  often  a  local  tenderness  of  the  scalp  and  cranium  which  may  be 
elicited  by  percussion,  and  in  most  cases  there  is  greater  tenderness  in 
that  part  of  the  cranium  lying  over  the  tumor. 

Vomiting  is  a  symptom  which  is  almost  as  frequent  as  headache. 
The  vomiting  is  often  of  a  projectile  character  and  not  accompanied  by 


TUMORS    OF    THE   BEAIN  457 

much  nausea.  Vomiting  occurs,  as  does  headache,  more  frequently' 
with  cerebellar  tumors.  It  is  associated  with  rapidly  growing  tumors, 
such  as  syphilitic  or  tuberculous  neoplasms. 

Vertigo  is  a  general  symptom  which  occurs  in  from  one-third  to  one- 
half  of  the  cases.  The  vertigo  may  be  slight,  such  as  is  often  felt  from 
ordinary  causes.  Occasionally  it  is  very  severe  and  accompanied  by 
forced  movements.  The  severer  forms  and  those  associated  with  forced 
movements  occur  with  tumors  of  the  cerebellum  and  the  parts  closely 
connected  with  it. 

Papilloedema  or  choked  disc  is  one  of  the  most  frequent  and  im- 
portant of  all  the  general  symptoms  of  brain  tumor;  it  occurs  at  some 
period  of  the  disease  in  at  least  four-fifths  of  the  cases,  more  frequently  in 
cerebellar  tumors  and  in  those  of  the  mid-brain  and  great  basal  ganglia. 
It  is  rare  in  tumors  of  the  medulla.  It  is  less  frequent  and  marked  in 
the  slow-growing  tumors  and  in  infiltrating  gliomata  of  the  hemispheres. 
The  condition  may  run  a  somewhat  rapid  course  and  then  improve  a 
great  deal  or  even  for  a  time  disappear;  but  ordinarily  the  course  is  pro- 
gressive and  it  ends  eventually  in  neuritis  and  an  atrophy  of  the  optic 
nerve.  Hence  the  examination  of  the  eyes  in  brain  tumors  should  be 
made  a  number  of  times  in  order  to  note  the  progress  of  the  trouble. 
Primary  atrophy  of  the  optic  nerve  does  not  occur  in  brain  tumors, 
except  to  a  certain  degree  in  some  frontal  tumors. 

The  choked  disc  is  caused  mainly  by  the  pressure  of  the  fluid  in  the 
subarachnoid  space,  which  space  communicates  with  the  connective- 
tissue  sheath  of  the  optic  nerve.  This  presses  the  nerve  upon  the  lamina 
cribrosa,  the  central  vein  of  the  retina  is  strangulated  and  oedema  and 
swelling  follow.  (Parker  states  that  the  choked  disc  is  due  to  a  dispro- 
portion between  the  intra-ocular  tension  and  the  intra-cranial  pressure, 
by  reason  of  which  the  disc  is  pushed  into  the  eye.)  Generally  there  is 
a  greater  degree  of  papilloedema  on  the  side  of  the  tumor. 

Slight  mental  defects  are  almost  always  present  in  tumors  of  the  brain. 
These  defects  consist  in  a  slowness  of  the  mental  processes,  a  condition 
of  hebetude,  a  tendency  to  attacks  of  somnolence,  and  sometimes  a 
peculiar  childishness,  silliness  and  tendency  to  foolish  joking.  The 
memory  is  also  usually  somewhat  weakened  and  the  power  of  attention 
lessened.  Such  psychical  defects  are  more  frequent  with  tumors  of  the 
frontal  lobes  and  more  frequent  also  with  large  tumors. 

General  convulsions  occur  in  about  one-fourth  of  the  cases  and  more 
frequently  when  the  tumors  are  situated  in  the  cerebral  hemispheres  and 
cortex.  There  may  be  also  apoplectiform  attacks,  from  which  the  patient 
recovers  in  the  course  of  a  few  days  or  weeks.  More  rarely  there  is  a 
genuine  apoplexy  from  the  bursting  of  a  blood-vessel  in  the  neighborhood 
of  the  tumor. 


458  DISEASES    OF   THE    NERVOUS    SYSTEM 

The  local  syinptomatology  of  cerebral  tumors  cannot  follow  always 
strictly  the  anatomical  subdivisions  of  the  brain.  There  are  symptoms 
distinguishing  tumors  which  lie  above  and  those  which  lie  below  the 
tentorium  because  the  pressure  conditions  are  not  alike. 


Fig.  217. — Showing  relationships  of  tumor  in  the  posterior  fossae  of  the  skull. 

In  suhtentorial  tumors  pressure  soon  blocks  the  aqueduct  of  Sylvius 
and  causes  a  hydrocephalus  and  pressure  symptoms.  Tumors  of  the 
hemispheres  cause  the  change  more  slowly,  consequently  optic  neuritis 
and  the  general  brain  symptoms  of  tumor  may  be  less  marked. 


TUMORS    OF    THE    BRAIN  459 

1.  Tumors  of  the  Prefrontal  Area. — Tumors  in  this  area  may  show  no 
locaHzing  symptoms.  Nevertheless  in  a  good  proportion  of  cases  some- 
thing characteristic  may  be  observed.  Sometimes  there  is  mental  dis- 
turbance, which  is  mainly  of  the  nature  of  mental  deterioration,  perhaps 
it  simulates  a  dementia  paralytica,  or  there  may  be  only  a  certain  degree 
of  fooHshness  and  silly  jocosity  ( Witzelkeit) .  The  pressure  of  a  frontal 
tumor  upon  the  olfactory  nerves  may  cause  disturbances  in  the  sense  of 
smell.  Pressure  on  the  optic  nerve  may  cause  disturbances  of  the  visual 
field  and  papilloedema.  But  the  pressure  on  the  optic  nerve  being  local 
and  direct  may  produce  at  the  same  time  an  early  atrophy  of  the  central 
fibres  shown  by  the  presence  of  a  central  scotoma  (Kennedy).  Rarely, 
the  tumor  involves  the  orbit  causing  paralysis  of  the  ocular  muscles  and 
protrusion  of  the  globe  of  the  eye.  If  the  tumor  grows  backward  there  is 
gradual  invasion  of  motor  centres  with  irritation,  showing  itself  by  local 
convulsions,  and  later  by  paralyses. 

Occasionally  in  frontal  tumors  there  is  tremor  of  the  hands,  and  a 
kind  of  ataxia  of  gait  and  station  (frontal  ataxia) . 

2.  Tumors  of  the  Precentral  Convolutions. — It  is  in  this  area  that  we 
are  often  able  to  make  the  closest  and  most  accurate  diagnosis  of  the 
localization  of  new  growths,  owing  to  the  involvement  of  the  different 
motor  centres.  These  centres  are  at  first  irritated,  with  the  result  of 
producing  local  spasms  or  Jacksonian  epilepsy.  Such  spasms  are  often 
preceded  by  sensory  symptoms  or  aurse.  As  the  tumor  grows,  the  area 
of  involvement  becomes  larger,  spasms  become  more  diffused,  and  gen- 
eral convulsions  may  finally  appear,  with  hemiplegia.  Besides  the 
symptoms  mentioned,  there  may  also  be  motor  aphasia  and  agraphia. 
If  the  tumor  is  subcortical  the  symptoms  are  more  of  the  paralytic  and 
spastic  type  and  less  of  a  convulsive  nature  than  when  the  cortex  is 
implicated. 

3.  Tumors  of  the  parietal  lobe  show  disturbances  of  sensation  and  of 
perception  tactile,  muscular  and  visual.  Tumors  in  the  anterior  portion 
(post-central  convolution)  cause  disturbances  of  cutaneous  sensation; 
those  in  the  superior  lobule  cause  astereognosis;  those  in  the  inferior 
lobule,  anteriorly  loss  of  deep  muscular  sense  with  ataxia;  those  further 
back  cause  forms  of  visual  imperception  such  as  apraxia  and  if  on  the  left 
side,  alexia. 

If  the  tumor  lies  deep  there  may  be  hemianopsia.  If  the  tumor  is  in 
the  post-central  we  get  with  disturbance  of  cutaneous  sensation,  usually 
some  motor  phenomena  due  to  irritation  of  the  precentral. 

4.  Occipital  Lobes. — Tumors  of  this  region,  if  situated  in  the  cuneus 
and  calcarine  fissure,  produce  homonymous  hemianopsia  partial  or  com- 
plete, the  macular  region  escaping.  If  the  tumor  involves  the  other  parts 
of  the  left  occipital  lobe  and  the  cuneus  is  not  seriously  involved,  there 


460  DISEASES    or    THE    NERVOUS    SYSTEM 

may  be  a  condition  known  as  soul  blindness,  sensory  apraxia  or  imper- 
ception  consisting  in  an  incapacity  to  understand  the  nature  of  the  things 
which  one  sees.  If  the  tumor  extends  up  chiefly  toward  the  angular 
gyrus,  on  the  left  side,  there  may  be  word  blindness,  along  with  some 
hemianopsia.  If  the  tumor  extends  farther  forward  and  deeply  into  the 
parietal  lobe,  there  will  be  hemiansesthesia,  hemiataxia,  and  perhaps 
a  little  hemiplegia  owing  to  involvement  of  the  fibres  of  the  internal 
capsule. 

Hallucinatory  symptoms  may  occur  in  occipital  lobe  tumors. 

5.  Temporal  Lobes-^The  temporal  or  temporo-sphenoidal  area  on  the 
right  side  is  very  nearly  a  latent  one.  On  the  left  side,  tumors  involving 
the  posterior  part  of  the  first  and  upper  posterior  part  of  the  second  tem- 
poral convolution  produce  sensory  aphasia. 

Tumors  of  the  anterior  and  inner  side  of  the  lobes  involving  the 
uncinate  and  hippocampal  gyri  may  produce  dreamy  states  and  disturb- 
ances of  smell  and  taste  (uncinate  fits).  Tumors  lying  further  back  may 
cause  also  third,  sixth  and  seventh  nerve  trouble  if  they  lie  in  the  ex- 
ternal portion,  but  if  posterior  and  internal  may  cause  nystagmus 
and  cerebellar  symptoms.  As  the  tumor  gets  deeper  it  may  cause 
hemiansesthesia  and  hemiplegia,  the  symptoms  of  paralysis  being 
more  marked  and  earlier  in  the  face  and  arm  (Kennedy). 

6.  Tumors  of  the  Corpus  Callosum. — Tumors  situated  in  this  area 
are  very  rare.  Their  symptoms  are  somewhat  characteristic  and  cor- 
respond somewhat  with  tumors  situated  in  the  ventricles  of  the  brain; 
in  other  words,  tumors  which,  beginning  in  the  central  parts  of  the  brain, 
gradually  extend  outward  toward  the  periphery.  The  symptoms  credited 
to  tumors  of  the  corpus  callosum  are  mental  dullness,  stupidity,  dys- 
praxia and  drowsiness,  the  patient  often  sitting  for  hours  mute,  re- 
fusing to  speak,  or  lying  in  a  half-somnolent  condition.  There  are  no 
paralyses  of  the  oculo-motor  or  other  cranial  nerves  and  often  no  optic 
neuritis,  or  any  severe  headache  and  vomiting.  There  is  no  anaesthesia. 
The  symptoms  progress;  locomotion  is  early  impaired  and  later  the 
patient  becomes  unequally  diplegic.  The  disease  gradually  progresses 
and  the  patient  dies  in  coma. 

7.  Tumors  of  the  Great  Basal  Ganglia  and  the  Capsule  (the  optico- 
striate  region). — The  general  symptoms  of  tumors  of  this  region  re- 
semble in  many  respects  those  of  tumors  of  the  corpus  callosum.  The 
hebetude,  however,  may  be  less  marked.  There  is  usually  a  progressive 
hemiplegia  which  may  be  accompanied  by  anaesthesia  and  sometimes 
by  choreic  movements,  if  the  tumor  involves  the  optic  thalamus  and 
adjacent  part  of  the  capsule. 

Tumors  of  the  corpus  striatum  cannot  be  diagnosticated  by  symptoms 
due  to  the  irritation  or  destruction  of  this  ganglion.     The  location  can 


TUMOKS    OF   THE   BRAIN  461 

be  only  approximately  estimated  by  the  presence  of  symptoms  due  to 
lesion  of  the  adjacent  parts,  viz.,  the  internal  capsule  and  the  adjacent 
motor  cortex.  When  on  the  left  side,  symptoms  of  aphasia  of  the  motor 
type  may  appear.  As  the  lesion  extends  there  may  be  hemiplegia,  and 
later,  perhaps,  irritative  symptoms  from  involvement  of  the  capsule  and 
motor  cortex. 

Tumors  of  the  Optic   Thalamus. — The  same  may  be  said  of  tumors 
here  as  of  those  of  the  corpus  striatum.     Lesions  of  the  thalamus  itself 


Fig.  218. — Showing  the  mechanism  of  crossed  paralysis.  Lesion  at  M  causes 
paralysis  of  third  nerve,  lesion  at  F  paralysis  of  fifth  nerve  with  hemiplegia  of  opposite 
side. 

give  no  specific  symptoms  unless  it  is  that  of  pain  referred  to  the  ex- 
tremities of  the  opposite  side.  But  by  extension  we  get  hemiansesthesia 
of  various  types  and  involvement  of  the  ocular  muscles  and  reflexes. 
There  is  later  even  homonymous  hemianopsia;  peculiar  forced  movements 
and  intention  tremor  may  occur.  The  opinion  that  in  lesions  of  the 
thalamus  there  is  a  paralysis  of  emotional  expression  has  been  sustained 
by  Mills.     The  thalamic  syndrome  which  is  observed  in  acute  lesions  of 


462  DISEASES    OF   THE    NERVOUS    SYSTEM 

this  ganglion  does  not  appear  very  characteristically  in  chronic  progressive 
lesions. 

Tumors  of  the  Pineal  Gland,  the  Pituitary  Body  and  Optic  Chiasm.— 

The  thalamus  and  adjacent  region  ('tween-brain  or  diencephalon)  is  a 
part  of  the  brain  which  in  man  is  not  sharply  limited.  It  may  be  divided 
into  an  upper  or  dorsal  part,  including  the  thalamus,  geniculate  bodies 
and  pineal  gland,  and  a  lower  or  ventral  part,  hypothalamus,  which  in- 
cludes the  corpora  mammillaria,  the  pituitary  body  and  infundibulum 
and  the  optic  chiasm.  Tumors  of  the  pineal  gland  are  generally  tera- 
tomata  or  psammomata.  They  may  cause  disturbance  of  metabolism 
leading  to  adiposity  and  precocious  mental,  physical  and  sexual  develop- 
ment. Secondarily,  they  cause  neighborhood  symptoms  such  as  disturb- 
ance in  ocular  movements,  optic  neuritis,  ataxia,  and  hydrocephalus 
from  blocking  the  aqueduct  of  Sylvius. 

Tumors  of  the  pituitary  body  may  be  associated  with  giantism  if  they 
occur  before  adolescence  and  ossification  of  the  epiphyses,  and  with 
acromegaly  if  they  occur  after  this  period.  As  they  grow  they  press  on 
the  chiasm  and  cause  optic  neuritis  and  atrophy  and  a  characteristic 
bitemporal  hemianopsia.  The  pituitary  disease  may  lead  to  other  dis- 
turbances of  nutrition  such  as  adiposity  and  increased  sugar  tolerance, 
andchanges  in  secondary  sexual  characters  forming  the  Frohlich  syndrome. 
(See  Acromegaly.) 

Tumors  of  the  Mid-brain. — The  mid-brain  includes  the  cerebral 
peduncles,  the  corpora  quadrigemina  and  the  aqueduct  of  Sylvius.  In 
the  base  of  the  peduncles  run  the  cerebrospinal  tracts,  above  which  is 
the  locus  niger  and  above  this  the  tegmentum  with  sensory  tracts,  the 
anterior  cerebellar  peduncles,  the  red  nuclei  and  the  nuclei  and  motor 
nerves  of  the  eye  (Fig.  213).  The  anterior  tubercles  of  the  corpora 
quadrigemina  and  geniculate  bodies  have  to  do  with  the  reflexes  and  co- 
ordination of  the  eye  movements,  the  posterior  with  the  functions  of 
the  eighth  nerve.  Tumors  here  are  sometimes  tumors  of  the  peduncles, 
and  sometimes  of  the  corpora  quadrigemina,  according  as  they  are 
superficial  or  deeply  situated.  The  general  character  of  the  symp- 
toms is  an  association  of  hemiplegia  with  disturbances  of  the  motility 
and  reflexes  of  the  eye,  often  ataxic  symptoms  and  sometimes  forced 
movements  and  disturbances  of  hearing.  We  would  expect  soon  to  get 
symptoms  of  ocular  palsies  and  of  brain  compression  from  closure  of 
the  aqueduct  of  Sylvius. 

As  many  as  six  different  groups  of  symptoms  or  syndromes  have  been 
described  due  to  lesions  here.  Some  of  these  are  given  under  the  head 
of  acute  softenings  and  hemorrhages.     (See  p.  443.) 

When  a  mid-brain  tumor  lies  in  a  cerebral  peduncle  it  produces 
"alternate  hemiplegia."     Thus  if  the  tumor  is  in  the  anterior  portion  and 


TUMOES    OF    THE    BRAIN  463 

situated  high  up,  there  is  a  palsy  of  the  third  nerve  on  one  side  and  a 
hemiplegia  of  the  opposite  side  (syndrome  of  Weber).  If  it  is  in  the  pos- 
terior portion  and  a  little  lower  it  will  cause  third  nerve  paralysis  on  one 
side  and  tremor  or  choreic  movements  on  the  other  (syndrome  of 
Benedict). 

Tumors  of  the  corpora  quadrigemina  cause  pupillary  inequalities  and 
paralyses,  oculo-motor  paralyses,  vertical  and  lateral  nystagmus.  If 
deep  enough  to  irritate  the  cerebellar  peduncle,  forced  movements, 
asynergy,  and  disturbance  of  equilibrium. 

Tumors  of  the  pons  cause  paralyses  of  cranial  nerves  on  one  side  and 
hemiplegia  on  the  other.  If  the  tumor  lies  near  the  fifth  nerve,  there 
may  be  a  palsy  of  this  nerve  on  one  side  and  hemiplegia  on  the  other  side 
(Fig.  218).     If  the  tumor  is  larger  it  may  produce  paralysis  of  the  fifth, 


STRATUM  GRISEUM 
CENTRALE 

AQU/CDUCTU3 

\CEREBR1 

MEDIAL- 
LONGITUDINAL  / 

BUNDLE       J„  .rrUH^^^'^^^k^  /^^^'^^^  LATERALtS 


NERVE  SULCUS  N.  OCULOMOTORII 

Fig.  219. — Section  through  mid-brain. 

sixth  and  seventh  nerves  on  one  side  and  hemiplegia  on  the  other  (syn- 
drome of  Gubler) .  If  situated  somewhat  superficially  and  on  the  lateral 
edge  of  the  pons  involving  the  peduncles,  there  will  be  forced  movements 
of  the  body,  either  toward  or  from  the  seat  of  the  lesion.  An  impor- 
tant sign  of  intra-pontile  tumor  (Spiller)  is  paralysis  of  lateral  associated 
movements  of  the  eyes.  If  the  tumor  is  unilateral  the  eyes  cannot  be 
turned  to  the  side  of  the  lesion. 

Tumors  of  the  medulla  are  rare  and  generally  tubercular  or  syph- 
ihtic.  The  medulla  is  the  seat  of  origin  of  the  IX,  X,  XI  in  part  and  XII 
nerves.  Through  it  run  motor  and  sensory  and  cerebellar  tracts.  It  is 
the  centre  for  the  automatic  regulation  of  respiratory,  cardiac  and  vaso- 
motor functions.  The  olivary  bodies  place  it  in  close  relation  also  with 
the  cerebellum.  Tumors  here  cause,  therefore,  paralyses  of  the  tongue, 
disturbances  of  deglutition,  speech  and  finally  of  respiration  and  cardiac 
action.     Hemiplegia,  hemiansesthesia  and  ataxic  symptoms  may  develop. 

Tumors  of  the  cerebellum  involve  often  a  study  of  the  condition 
of  the  vestibular  nerve,  of  the  spinal  apparatus  of  equilibrium,  and  of 


464 


DISEASES    OF    THE    NERVOUS    SYSTEM 


the  cerebro-cerebellar  connections.  It  involves  the  employment  of 
the  diagnostic  tests  previously  given.  The  accompanying  diagram  of 
the  cerebellar  connections,  modified  from  Thomas  and  made  more  com- 
plete by  Dr.  W.  F.  Schaffler,  will  be  found  useful. 


smioR  muiiai.. 

CEKBaW-^ESWmilT^KT. 

mniNTH. 


MmLE  VCWHCLE 

i[smuLo  s?wLTmr. 


Post.  Column  fiucUi. 


Cm  mi  Cond 


FlLltT. 

OLIVE. 


CoLmii  Of  GoLi. 
CoLmn«<^imfiCH. 


Fig.  220. — Connections  of  the  cerebellum  witli  cerebral  cortex,  vestibular  nerve  and 

spinal  cord.     (Schaller.) 


Tumors  of  the  cerebellum  are  more  often  seen  in  children  and 
they  grow  rather  rapidly,  so  that  a  distinct  picture  of  cerebellar  dis- 
ease may  be  developed  in  a  few  months.  The  early  symptoms  are 
vomiting,  headache  and  choked  disc ;  and  the  child  may  be  first  brought 
to  the  physician  for  stomach  trouble.  The  stumbling  ataxic  gait  then 
develops   and  with  it   a   good  deal  of   general  muscular  weakness   or 


TUMORS    OF   THE   BRAIN 


465 


parasthenia.  Strabismus  and  nystagmus  are  often  early  symptoms. 
The  patient  has  a  weakness  of  one  side  not  amounting  to  hemiplegia 
and  there  may  be  some  facial  nerve  weakness  on  the  same  side  as 
the  lesion.  There  is  diminution  or  loss  of  deep  reflexes  and  some  hypo- 
tonia. As  the  ataxia  progresses,  the  patient  may  be  unable  to  stand 
well,  but  inclines  to  fall  backward  or 
to  one  side;  when  he  tries  to  sit,  even, 
he  may  fall  over  and  the  hands  be- 
come awkward  and  ataxic,  though 
less  so  than  the  legs.  There  may  be 
sudden  seizures  of  violent  vertigo, 
or  loss  of  consciousness,  with  tonic 
irregular  movements  of  the  limbs,  or 
perhaps  only  sudden  short  forced 
movements,  throwing  the  patient  to 
the  floor  (cerebellar  seizures).  These 
are  less  common  in  children  than  in 
adults.  Other  special  symptoms  of 
cerebellar  disease  elsewhere  described 
may  appear.  These  are  nystagmus, 
jerky  tremors  of  the  hands,  adiado- 
kokinesis,  asynergy  in  locomotion, 
dysmetria,  cerebellar  catalepsy  and 
the  disturbance  of  the  normal  laby- 
rinthine reflexes  as  shown  by  Barany 
tests  (see  general  diagnosis). 

As  the  tumor  grows  it  usually 
stops  up  the  aqueduct  from  the  third 
to  the  fourth  ventricle,  and  then  an 
internal  hydrocephalus  develops  and 
we  get  symptoms  of  brain  compres- 
sion. The  mind  becomes  apathetic 
and  slow;  headache  and  vomiting  are 
less,  blindness  sets  in,  with  paralysis 
of  some  of  the  motor  nerves  of  the  eye 
and  dilated  and  fixed  pupils.  The 
neck  is  retracted  and  stiff  and  Kernig's  sign  is  present.  The  pulse  may  be 
slow  at  first  and  later  in  the  terminal  stage  may  be  signs  of  bulbar  com- 
pression and  paralysis.  The  patient  emaciates  and  death  occurs  in  one- 
half  to  two  years ;  though  in  some  slow-growing  tumors  of  adults  the  dis- 
ease may  last  ten  years  or  more. 

Tumors  of  the  lateral  lobes  of  the  cerebellum  should  theoretically 
cause  especially  ataxia  of  the  extremities,  on  the  same  side  and  a  tendency 

30 


Fig.  221.- — Attitude  in  a  case  of 
cerebellar  tumor. 


466 


DISEASES    OF    THE    NERVOUS    SYSTEM 


to  fall  to  that  side.  Tumors  of  the  vermis  should  cause  more  disturbance 
of  equilibrium  and  cause  a  tendency  to  fall  usually  forward  or  backward. 
Tumor  of  the  ponto-cerebellar  angle  gives  a  rather  special  sympto- 
matology. It  arises  usually  as  a  small  fibroma  on  the  auditory  nerve. 
It  grows  very  slowly  and  may  undergo  finally  sarcomatous  degenera- 
tion. As  it  grows  it  forms  a  hard,  circumscribed,  pedunculated  mass 
pressing  into  the  angle  between  the  lateral  and  anterior  surface  of  the 
pons  and  the  middle  peduncle  of  the  cerebellum.  The  first  symptoms 
are  simply  those  of  irritation  and  compression  of  the  eighth  nerve,  with 
tinnitus,  vertigo,  and  progressive  deafness;  then  there  may  be  pains  in 
the  trigeminal  nerve  and  later  perhaps  some  parsesthesia  or  anaesthesia 


Fig.  222. — P(j.sitiuii  of  head  in  cerebellar  tumor.      {Fraenkel.) 

over  the  distribution  of  this  nerve  with  loss  of  conjunctival  reflex.  The 
facial  nerve  may  become  involved  as  the  disease  progresses.  Usually 
not  till  after  several  years  does  the  patient  begin  to  show  the  general 
symptoms  of  brain  tumor,  and  then  those  of  cerebellar  disease:  headache, 
vomiting,  choked  disc,  staggering,  cerebellar  gait,  falling  generally  to  the 
side  of  the  lesion,  cerebellar  attitude.  In  about  half  the  cases  there  are 
cerebellar  seizures  and  there  may  be  some  hemiplegia  on  the  side  of  the 
lesion;  finally,  symptoms  of  internal  hydrocephalus  and  brain  pressure 
appear. 

Multiple  Tumors. — About  one-tenth  of  all  cases  of  brain  tumor  are 
multiple.  Hence,  in  making  a  diagnosis  of  the  localization  of  tumors 
this  fact  must  be  borne  in  mind.  The  tumors  which  are  most  frequently 
multiple  are  tubercle,  cancer,  and  melanotic  growths. 


TUMORS    OF    THE    BRAIN  467 

Pathology. — Tubercle  is  the  form  of  tumor  found  oftenest  in  children. 
It  is  more  often  located  in  the  cerebellum,  but  may  appear  in  the  pons 
or  other  parts  of  the  brain.  It  may  be  a  single  or,  as  it  is  then  called,  a 
solitary  tubercle,  or  there  may  be  a  multiple  growth.  The  tumor  is 
irregularly  round  in  shape  and  varies  in  diameter  from  one  and  a  half  to 
two  inches.  It  has  a  grajdsh-j^ellow  appearance  externally;  internally, 
a  yellowish  or  cheesy  look.  It  is  not  vascular,  but  is  often  surrounded 
by  softened  or  inflamed  tissue.  There  may  be  an  associated  meningitis. 
The  tumors,  when  solitary,  usually  start  from  the  central  parts  of  the 
brain,  but  they  also  develop  on  the  meninges  of  the  convexitN'',  particularly 
in  the  parietal  region,  and  sometimes  they  develop  also  at  the  base. 
The  tumors  develop  usually  from  some  infectious  focus,  starting  in  a 
blood-vessel  of  the  pia  mater.  Microscopically,  the  tumor  shows  the 
ordinary  appearances  of  tuberculous  growths.  It  contains  in  its  periphery 
many  round  cells,  nuclei,  and  giant  cells.  In  the  centre  there  is  usualty 
an  amorphous  substance,  the  product  of  degeneration  and  the  breaking 
down  of  the  ordinary  substance  of  the  tumor.  The  characteristics  of 
the  growths  are  the  presence  of  the  round  cells  and  giant  cells,  the  casea- 
tion and  softening  of  the  centre,  and  the  absence  of  vascularization,  with 
the  presence  of  the  bacilli. 

Syphiloma  or  Gumma. — Gummatous  tumors  of  the  brain  are  usually 
associated  with  syphilitic  meningitis  and  endarteritis  and  are  usually 
found  upon  the  brain  surface,  oftenest  on  the  base,  next  upon  the  con- 
vexity of  the  frontal  and  central  convolutions.  The  process  appears 
either  in  the  form  of  a  somewhat  distinct  tumor  or  in  the  form  of  an  ir- 
regular thickened  exudate  lying  upon  the  surface  of  the  brain  and  forming 
what  is  called  gummy  meningitis.  The  gummata  may  attain  great  size. 
They  start  usually  from  the  pia  mater  and  are  due,  as  in  the  case  of  tuber- 
cle, to  the  irritative  action  of  the  infective  organism.  The  gumma  is 
irregular  in  shape;  it  has  a  somewhat  thick,  grayish  periphery  and  often  a 
yellowish  centre,  the  appearances  differing  with  the  age  of  the  tumor. 
Microscopically,  it  is  found  to  consist  of  small  round  cells  and  spindle 
cells  with  various  broken-down  nerve-tissue  elements.  Gummata  are 
at  the  present  time  very  rare  forms  of  brain  tumor,  as  their  development 
is  usually  controlled  by  treatment. 

Actinomycosis  is  a  form  of  infectious  tumor  which  sometimes  ex- 
tends from  the  face  and  neck  into  the  brain,  leading  to  inflammatory 
processes,  however,  rather  than  to  true  tumors.  No  other  neoplasms 
of  infectious  origin  attack  the  brain  unless  sarcoma  be  found  to  be  of 
that  nature. 

Cystic  tumors  are  not  uncommon  and  are  the  result  of  parasitic  in- 
vasion, of  injuries,  and  of  the  breaking  down  of  a  glioma  or  from  a 
teratoma. 


468  DISEASES    OF   THE    NERVOUS    SYSTEM 

Glioma  is  the  most  frequent  form  of  brain  tumor.  It  may  occur  in 
any  part  of  the  brain,  but  is  most  frequently  found  in  the  cerebrum. 
It  is  the  only  tumor  which  is  peculiar  to  the  nervous  centres,  being 
developed  from  the  neuroglia  tissue  which  forms  the  supporting  structure 
of  these  centres.  Glioma  originates  in  the  white  or  gray  matter  of  the 
nerve-centres  and  not  from  the  membranes  or  fibrous  structures.     It  may 


Fig.  223.— Tumor  of  frontal  lobe.     (J.  R.  Hunt.) 

grow  to  a  very  large  size  and  is  the  form  of  brain  tumor  which  becomes 
the  largest.  Gliomatous  tumors  measure  from  three  to  eight  or  more 
centimetres  in  diameter.  In  appearance  the  glioma  can  be  scarcely 
distinguished  from  the  brain  substance  itself,  but  usually  looks  like 
either  pale  or  congested  gray  matter,  or  it  may  have  a  yellowish  or 
gelatinous  appearance.  The  tumor  is  very  vascular  and  it  may  show 
the  results  of  hemorrhages.     The  central  part  sometimes  breaks  down, 


TUMORS    OF    THE   BRAIN SYPHILIS 


469 


forming  cavities  or  cysts.  The  tumor  may  grow  very  rapidly,  infiltra- 
ting the  normal  tissue  and  in  these  cases  there  is  hardly  any  definite 
boundary  between  it  and  the  normal  tissue.  In  other  cases  the  tumor 
grows  slowly,  but  rarely  if  ever  becomes  en  capsuled.  Microscopically, 
it  is  found  to  consist  of  small  cells  with  delicate  fibrous  prolongations, 


Fig.  224. — Tumor  of  cerebello-pontine  angle. 


these  being  the  glia  cells.  Gliomata  may  undergo  certain  changes, 
e.g.,  a  mucous  degeneration  of  the  cells  takes  place,  forming  a  myxo- 
glioma.  When  there  is  with  the  neuroglia-cell  proliferation  a  rich 
proliferation  of  round  cells  from  the  connective  tissue,  it  is  called  a  glio- 


470  DISEASES    OF    THE    NERVOUS    SYSTEM 

sarcoma.  When  the  tumor  is  situated  near  the  surface,  involves  the 
membranes,  and  grows  slowly,  with  an  increase  in  fibrous  tissue,  it  is 
called  a  fibro-glioma.  When  the  gliomatous  growth  is  very  firm  and 
hard,  the  fibrous  portion  of  the  glia  tissue  predominates;  it  constitutes  a 
nodule  such  as  is  found  in  multiple  sclerosis,  and  these  hard  gliomata 
are  sometimes  called  neuro-gliomata. 

Sarcoma. — The  sarcoma  and  its  various  modifications  is  next  to 
glioma  in  frequency.  It  may  be  primary  or  secondary  in  origin.  The 
sarcoma  develops  from  the  brain  membranes  or  from  the  walls  of  the 
blood-vessels  and  nerve  sheaths.  Sarcomata  may  be  single  or  multiple. 
They  may  be  of  all  shapes  and  they  grow  often  rapidly  to  very  varying 
sizes.  They  often  develop  a  capsule.  They  are  white  or  grayish  in 
appearance  or  may  be  somewhat  yellowish,  dependent  on  the  predomi- 
nance of  the  different  kinds  of  cells  and  blood-vessels.  Microscopically, 
they  are  made  up  of  small  round  cells,  spindle  cells,  and  other  cells  of 
various  sizes  and  forms.  They  contain  often  considerable  fibrous  tissue. 
They  contain  blood-vessels,  but  are  not  richly  vascular.  The  essential 
characteristic  of  the  sarcoma  is  the  rich  development  of  round  cells  and 
spindle  cells;  in  other  words,  its  rich  cellular  contents.  Sarcomata  are 
peculiar  in  undergoing  many  modifications.  Thus  sometimes  fibrous 
tissue  develops  largely  and  the  tumor  is  called  a  fibro-sarcoma;  sometimes 
the  tumor  undergoes  mucous  degeneration  and  is  called  a  myxo-sarcoma. 
There  may  be  a  breaking  down  of  the  centre  with  the  formation  of  cysts. 
There  may  be  a  development  of  pigment.  Not  frequently  a  sarcoma- 
tous process  invades  a  glioma  and  we  have  a  mixture  of  a  sarcoma  and 
glioma.  Sarcomatous  tumors  sometimes  have  an  alveolar  structure. 
These  tumors  contain  endothelial  cells  derived  from  the  lymphatics. 
When  sarcomata  develop  from  the  dura  mater  and  are  slow  in  growth 
there  may  be  calcareous  deposits  in  them  and  they  are  called  psam- 
momata. 

Endothelioma  develops  from  the  endothelium  of  the  blood-vessels  and 
lymphatic  spaces.  It  usually  starts  from  the  meninges  and  is  often  en- 
capsulated and  therefore  subject  to  surgical  treatment. 

The  fibroma  is  a  very  rare  brain  tumor,  unless  the  Pacchionian  bodies, 
when  enlarged  and  hardened,  may  be  so  considered.  Occasionally  fibro- 
neuromata  are  found  developing  on  the  roots  of  the  cranial  nerves. 

Osteoma  is  not  particularly  rare,  developing  in  the  form  of  bony 
plates  in  the  dura,  falx,  or  tentorium.  Osteomata  in  the  brain  substance 
are  mere  pathological  curiosities. 

Angiomata  occasionally  occur  in  the  pia  mater  in  connection  with 
vascular  nsevi  of  the  face,  and  also  in  the  cortex  and  basal  ganglia.  They 
are  also  usually  congenital. 

Enchondromata  and  lipomata  are  extremely  rare. 


TUMOES    OF    THE    BRAIN SYPHILIS  471 

Cancer  is  relatively  a  rare  affection  of  the  brain,  and  is  almost  always 
of  secondary  origin. 

Parasitic  growths. — Parasitic  tumors  are  extremely  rare  in  this  coun- 
try. The  forms  which  are  found  are  the  echinococcus  and  the  cysticercus 
cellulosse.  The  echinococcus  produces  hydatid  cysts,  which  may  be 
large  or  small,  few  or  many,  and  are  usually  all  upon  the  surface  of  the 
brain.  T  hey  are  much  rarer  than  the  cysticerci.  These  latter  form  cysts 
which  are  usually  multiple,  slow  in  growth,  lie  upon  the  surface  of  the 
brain  or  in  the  ventricles,  are  encapsuled,  and  show  no  symptoms. 

Aneurisms  are  anatomically  tumors,  but  clinically  they  present  some 
special  symptoms  and  hence  are  described  separately. 

Diagnosis. — -It  is  necessary  first  to  make  the  diagnosis  of  the  presence 
of  the  tumor,  next  of  its  location,  and  finally  of  its  nature.  The  existence 
of  a  brain  tumor  is  determined  by  the  presence  of  the  characteristic 
general  symptoms — ^headache,  vomiting,  vertigo,  optic  neuritis,  mental 
disturbances,  progressive  course  and  local  signs.  The  things  which  pro- 
duce somewhat  similar  symptoms  are  localized  meningitis  (syphilitic  or 
tubercular),  brain  abscess,  localized  foci  of  arterial  sclerosis;  lead  poison- 
ing, hysteria,  acute  internal  hydrocephalus  and  certain  toxaemias. 

The  physician  must  bear  in  mind  the  age  of  the  patient  and  the  exist- 
ence of  a  tuberculous  or  syphilitic  history,  the  history  of  an  injury,  of 
local  tenderness,  and  the  presence  of  some  new  growth  in  other  parts  of 
the  body,  particularly  about  the  neck  or  thorax  or  in  the  lungs. 

Blood  tests  assist  in  excluding  inflammatory  and  luetic  conditions. 
Lumbar  puncture  and  examination  of  the  cerebrospinal  fluid  helps  to 
determine  lues  and  meningitis;  brain  puncture  and  the  withdrawal  of 
a  very  small  cylinder  of  brain  tissue  which  may  be  examined  microscopic- 
ally has  become  a  useful  and  safe  operation.  Percussion  of  the  skull 
sometimes  shows  a  duller  note  over  the  region  of  a  tumor.  Occasionally 
in  young  patients  percussion  brings  out  a  cracked-pot  sound.  This  only 
occurs  when  the  intra-cranial  pressure  has  loosened  the  sutures  of  the 
skull.  In  X-ray  pictures  one  sometimes  can  see  a  darkened  mass  indicating 
the  presence  of  a  tumor.  More  often  the  X-ray  only  helps  by  showing 
changes  in  the  bone,  as  in  tumors  of  the  sella  turcica.  Sometimes  also 
in  superficially  placed  tumors  the  plate  shows  broad  lines  indicating  dila- 
tations of  the  veins  of  the  diploe. 

The  diagnosis  of  the  location  of  the  tumor  is  based  upon  the  rules 
already  given  in  regard  to  local  diagnosis. 

The  diagnosis  of  the  nature  of  the  tumor  can  often  be  made  and  should 
be  attempted.  About  two-thirds  of  tumors  in  adults  are  gliomata. 
Tubercle  and  glioma  are  the  most  common  in  children.  Cerebellar 
tumors  are  often  gliomata,  especially  in  adults.  Tumors  of  the  ventricles 
are   usually   gliomata   or   adenomata.     Tumors   that   develop   without 


472  DISEASES    OF   THE    NERVOUS    SYSTEM 

many  serious  pressure  symptoms  are  usually  gliomata.  Cancers  are 
practically  always  secondary  and  sarcomata  sometimes.  Endothelioma 
are  generally  superficial,  at  first,  starting  from  the  meninges.  The  pres- 
ence of  syphilitic  tumors  can  be  inferred  from  laboratory  tests.  Sudden 
exacerbations  of  symptoms  due  to  intra-neoplasmic  hemorrhage  suggest 
glioma. 

Prognosis. — In  extremely  rare  cases  tumors  of  the  brain  appear  to 
stop  growing  and  become  encapsulated  and  atrophied.  Such  tumors 
are  of  a  tuberculous  or  syphilitic,  perhaps  sometimes  of  a  gliomatous  or 
sarcomatous,  character.  As  a  rule,  the  brain  tumor  grows  steadily  and 
the  symptoms  of  the  disease  become  more  pronounced  until  death  occurs. 
The  prognosis  is  best  for  tubercle  in  children  and  gumma  in  adults.  It  is 
worse  in  cases  of  glioma  and  cancer.  The  disease  lasts  on  an  average 
two  or  three  years,  ranging  from  a  month  to  eighteen  years. 

Treatment. — Something  can  be  done  medically  in  cases  of  tuberculous 
tumors,  syphilitic  tumors,  and  possibly  in  the  sarcomatous  variety.  In 
tuberculous  tumors  a  general  constitutional  and  strengthening  treatment 
must  be  resorted  to;  fresh  air,  rest,  tonics,  and  proper  food  being  the  main 
reliance.  In  sarcoma  and  glioma,  some  help  may  be  obtained  from  the 
internal  use  of  arsenic.  Iodide  of  potassium  sometimes  helps  non-syphi- 
litic tumors.  Symptomatically  we  must  give  drugs  for  the  relief  of  pain. 
The  ice  cap  and  leeching  often  help  the  headache.  Should  convulsions 
develop,  the  bromides  should  be  used,  just  as  in  idiopathic  epilepsy. 

In  cases  in  which  the  location  of  the  tumor  can  be  made  out,  the  ques- 
tion of  surgical  interference  should  be  considered.  The  percentage  of 
cases  in  which  surgery  can  effectually  help  is  small.  It  will  include  only 
those  cases  in  which  the  tumor  can  be  located;  of  those  which  can  be 
located,  only  those  which  are  in  an  accessible  region,  and  finally,  of  those 
which  are  in  an  accessible  region,  it  includes  those  whose  removal  will 
not  leave  the  patient  helpless,  demented  or  aphasic.  The  removable 
tumors  of  the  brain  amount  to  less  than  5  per  cent.  They  are,  in  par- 
ticular, the  endotheliomata,  sarcomata  and  gliomata.  These  latter  some- 
times degenerate  and  become  absorbed  after  partial  removal.  Tumors 
can  be  removed  with  possible  benefit  from  the  superficial  part  of  any 
portion  of  the  cerebral  hemispheres  except  the  left  temporal  lobe.  Here 
the  patient  if  operated  on  would  be  made  aphasic  and  probably  hemi- 
plegic.  Tumors  can  be  removed  from  the  cerebellum  and  the  cerebello- 
pontine angle  with  occasional  success  and  even  with  brilliant  results. 
Tumors  can  be  removed  from  the  hypophysis,  by  the  very  expert. 
Tumors  of  the  mid-brain,  pons,  medulla,  and  of  the  ventricles  are  not 
operable.  In  cases  which  are  not  operable,  the  decompressive  operation 
of  Gushing  or  puncture  of  the  corpus  callosum  may  often  be  done  with 
advantage. 


TUMORS    OF    THE    BRAIN SYPHILIS  473 

Lumbar  puncture  can  be  employed  to  test  and  to  a  slight  extent 
relieve  the  intra-cranial  pressure.  The  measure  should  not  be  employed, 
however,  in  subtentorial  tumors  as  the  medulla  may  be  pushed  into  the 
foramen  magnum  and  death  ensue.  The  ordinary  pressure  of  the  cere- 
brospinal fluid  of  40  to  150  mm.  of  water  may  in  brain  tumor  be  increased 
to  250  and  900. 

INTRA-CRANIAL  ANEURISMS 

Intra-cranial  aneurisms  are  of  two  kinds — ^" miliary"  and  those  of 
large  size.  The  miliary  aneurisms  are  minute  dilatations  of  the  vessels 
and  are  always  multiple;  they  have  been  described  under  the  head  of 
cerebral  hemorrhage.  Large  aneurisms  affect  only  the  large  cerebral 
arteries  at  the  base  of  the  brain.  The  arteries  are  affected  in  the  following 
order:  middle  cerebral,  basilar,  internal  carotid,  and  anterior  cerebral. 
The  anterior  and  posterior  communicating  and  vertebral  arteries  are 
occasionally  involved,  the  posterior  cerebral  and  inferior  cerebellar  very 
rarely  (Gowers). 

Etiology. — Males  are  affected  slightly  oftener  than  females.  Aneu- 
risms occur  at  all  ages  from  ten  to  sixty;  before  ten  and  after  sixty  they 
are  extremely  rare.  Heredity  occasionally  plays  a  part  in  predisposing 
to  cerebral  aneurisms.  The  exciting  causes  are  embolism,  especially 
when  the  emboli  contain  microbes,  syphilitic  disease,  injuries,  and  in 
rare  cases  senile  arterial  degeneration. 

The  symptoms  are  very  indefinite;  they  resemble  to  a  considerable 
extent  those  of  tumor  at  the  base  of  the  brain;  headache  and  vertigo, 
mental  dullness  and  irritation,  cranial-nerve  palsies,  and  occasionally 
hemiplegia  and  convulsions  are  noted.  Optic  neuritis  is  rather  rare.  In 
a  few  cases  the  patient  is  conscious  of  a  murmur  or  recognizes  the  pul- 
sating sensation  in  the  head.  Sometimes  when  the  aneurism  is  in  the 
vertebral  artery,  a  murmur  can  be  heard  between  the  mastoid  process 
and  the  spinal  column  (Moser). 

The  diagnosis  is  often  difficult;  it  is  based  on  symptoms  of  tumor  at 
the  base  of  the  brain  pressing  on  cranial  nerves  and  on  motor  or  sensory 
tracts.     The  effect  of  carotid  compression  should  be  tried. 

The  prognosis  is  not  good.  In  perhaps  the  majority  of  cases  a  rup- 
ture of  the  vessel  occurs  in  a  few  years;  however,  rupture  is  not  the  in- 
evitable event,  and  sometimes  the  disease  becomes  stationary  or  under- 
goes spontaneous  cure. 

The  treatment  of  the  disease,  if  it  can  be  recognized,  is  the  same  as 
that  for  aneurism  elsewhere,  so  far  as  drugs  are  concerned.  The  use  of 
salvarsan  has  produced  good  results;  surgically,  the  common  carotid  may 
be  tied  (though  this  involves  some  risk)  and  perhaps  the  vertebral  if  the 
aneurism  is  believed  to  be  connected  with  that  artery  or  with  the  basilar. 


CHAPTER  XX 

FUNCTIONAL  AND  DEGENERATIVE  DISEASES- 
EPILEPSY 

Functional  is  a  term  applied  to  nervous  diseases  in  which  no  known 
anatomical  change  underlies  the  morbid  phenomena.  Degenerative 
diseases  are  those  due  to  or  associated  with  a  constitutional  deterioration, 
or  biogenetic  defect.  The  number  of  diseases  of  functional  character 
is  steadily  lessening,  and  the  use  of  the  term,  therefore,  is  being  supplanted 
by  other  qualifying  words. 

Epilepsy  is  a  disease  of  the  functional  and  degenerative  type,  although 
the  essential  and  dominant  symptoms  are  due  to  various  morbid  condi- 
tions. It  is  a  chronic  nervous  disorder  characterized  by  periodical 
seizures  attended  by  loss  of  consciousness  and  usually  by  convulsions. 
Mental  disturbances  may  accompany  or  take  the  place  of  the  convul- 
sions. The  mental  make-up  of  the  patient  is  generally  peculiar  and  if 
the  disease  progresses  some  mental  deterioration  sets  in.  It  has  no  estab- 
lished pathological  anatomy,  although  there  are  degenerative  cell  changes 
in  the  brain  cortex. 

Symptomatic  epilepsy  is  a  form  in  which  the  periodic  convulsive 
attacks  are  associated  with  gross  organic  changes  in  the  brain,  or  is  the 
expression  of  a  definite  epileptogenous  irritation  (toxic,  vascular,  psychic 
or  reflex). 

Jacksonian  or  partial  epilepsy  is  a  form  of  epilepsy,  usually  sympto- 
matic, and  is  characterized  by  periodic  convulsions  affecting  only  certain 
groups  of  muscles,  and  often  unattended  by  loss  of  consciousness. 

Hystero-epilepsy  is  not  epilepsy,  but  a  form  of  hysteria. 

Eclampsia  or  acute  epilepsy  is  the  name  given  to  a  single  isolated 
attack  of  convulsions.     It  is  generally  of  the  symptomatic  type. 

Ordinary  or  "idiopathic"  epilepsy  shows  itself  in  three  rather  dis- 
tinct types  of  attacks,  viz.,  that  of  severe  attacks  called  the  grand  mal; 
that  of  minor  attacks,  the  petit  mal;  and  the  rare  larvated  forms  char- 
acterized by  acute  mental  disorder  and  called  psychical  epilepsy  or  the 
psychical  epileptic  equivalent. 

Etiology. — Predisposing  causes:  Heredity  is  the  most  potent  of 
any  single  influence.  A  history  of  epilepsy,  insanity  or  some  serious 
neuropathic  condition  is  found  in  the  family  in  over  one-third  of  the 
cases  and  rather  more  on  the  paternal  side. 

474 


FUNCTIONAL    AND    DEGENERATIVE    DISEASES  475 

In  many  other  cases  it  can  only  be  established  that  the  family  is  a 
neuropathic  one.  The  heredity  is  rarely  direct;  i.e.,  the  parents  are  not 
epileptic  in  more  than  about  1  per  cent,  of  cases.  Alcoholism  and  the 
intermarriage  of  neurotic  persons  contribute  to  produce  the  convulsive 
tendency  in  children.  The  element  of  alcoholism,  in  my  experience 
(private  and  public)  is  only  about  5  per  cent.  It  must  be  remembered 
that  many  parents  reported  alcoholic  were  not  so  at  the  time  of  the  birth 
of  the  child.  Powerful  emotions  during  pregnancy,  accouchement  in- 
juries, and  syphilis,  have  slight  influence.  The  Wassermann  test  for 
syphilis  in  epileptics  has  brought  out  a  small  percentage  of  positive  re- 
actions. Very  important  causes  of  epilepsy  are  cerebral  or  meningeal 
hemorrhage  and  attacks  of  encephalitis  occurring  in  early  life.  Such 
attacks  may  lead  to  mental  defects  and  paralysis;  about  40  per  cent,  of 
these  cases  have  epilepsy. 

More  cases  occur  in  the  country  than  the  city,  more  in  temperate 
climates,  and  more  among  in-bred  races.  American  statistics  show 
a  slight  preponderance  among  males.  The  epileptic  age  is  between 
birth  and  twenty,  and  still  more  definitely  between  five  and  fifteen. 
In  three-fourths  of  the  cases  the  disease  begins  before  the  age  of 
twenty;  in  one-sixth  of  my  cases,  before  the  age  of  five.  After 
twenty  the  danger  of  epilepsy  is  slight,  and  when  it  occurs  it  is 
usually  due  to  accidental  causes,  like  syphilis,  alcoholism,  or  plumb 
ism.  Idopathic  epilepsy,  however,  may  develop  even  after  sixty.  The 
accompanjdng  table  shows  graphically  the  relation  of  age  to  the  de- 
velopment of  epilepsy,  chorea,  and  neuralgias. 

Exciting  causes  are  not  present  in  the  majority  of  cases.  The 
most  important  are  the  occurrence  of  rickets  at  the  time  of  denti- 
tion, injury  to  the  head,  sunstroke,  acute  infectious  diseases  and 
toxaemias,  persistent  reflex  irritations  and  alcoholism.  The  impor- 
tance of  traumatism  when  there  has  been  a  real  injury  to  the  brain  is 
considerable.  Simple  concussions  without  organic  injury  do  little  harm. 
Masturbation  is  a  real  but  rare  exciting  cause.  The  so-called  reflex 
causes  are  ocular  and  auditory  irritations,  worms,  gastro-intestinal  weak- 
ness, dental  irritations,  and  lesions  involving  peripheral  nerves.  Probably 
the  gastro-intestinal  tract  and  genital  organs  furnish  the  most  important 
exciting  irritations. 

X-ray  examination  often  shows  some  defects  in  the  position  and 
functioning  of  the  digestive  tube  with  ptosis,  kinks  and  a  patent  ileo- 
csecal  valve. 

A  chronic  epilepsy  may  be  brought  out  by  peripheral  irritations  while 
more  rarely  there  occurs  only  a  reflex  epileptiform  neurosis,  the  convul- 
sions subsiding  when  the  irritation  is  removed. 

Epileptic  seizures  of  characteristic  type  may  be  caused  by  psychic 


476 


DISEASES    OF   THE    NERVOUS    SYSTEM 


states.  In  other  words,  an  apparent  epilepsy  may  be  psychogenous. 
Some  followers  of  psychoanalysis  claim  that  the  convulsive  seizure 
itself  is  the  expression  of  a  suppressed  wish  or  instinct  of  infantile  origin. 
Symptoms. — The  Onset. — The  disease  begins  sometimes  with  attacks 
of  petit  7nal  which  may  last  one  or  more  years  before  anything  more 
serious  occurs.  Then  suddenly  there  is  a  convulsion.  Occasionally 
nothing  but  petit  mat  attacks  ever  occur.  In  other  cases  without  pre- 
vious warning  the  patient  has  a  severe  seizure.  In  six  months  or  a  year 
he  has  another,  in  the  next  year  he  has  three  or  four  and  then  they  come 
on  regularly  every  week  or  two. 


Percentage 

of 
total  cases 

60;^ 

50% 
40  X 
30% 
20% 

lO/o 

up  to 
end  of 
5Vr 

6'^ 

to 

7th 

lit 

to 

to 

3M.* 
to 

4o*^ 

4  p.' 
to, 

51^.' 
to 

60*^ 

to 

r '' 

"^. 

/ 

\ 

r 

u 

^^ 

N 

\ 

\ 

1 

1/ 

/ 

\ 

V 

:i; 

^ 

v.. 

...^ 

Fig.  225. — Table  showing  percentage  of  cases  of  epilepsy,  chorea,  and  neuralgia 
occurring  at  each  half -decade  and  (after  twenty)  each  decade.  Double  line,  epilepsy; 
dotted  line,  chorea;  single  line,  nuralgia. 

The  Convulsion. — The  patient  often  feels  some  premonitory  symp- 
toms for  a  few  hours  or  a  day,  consisting  of  general  malaise,  irritability, 
or  giddiness.  The  attack  begins  in  about  half  the  cases  with  a  peculiar 
sensation  called  the  aura.  Often  also  a  loud  cry  is  uttered  and  the 
patient  falls  unconscious  to  the  ground.  The  face  is  pale,  the  eyes  are 
open  and  turned  up  or  to  one  side,  and  the  pupils  dilated.  The  head 
is  drawn  back  or  to  one  side,  and  the  whole  body  is  in  a  state  of  rigidity 
or  tonic  spasm.  The  arms  are  slightly  drawn  out  from  the  trunk,  the 
forearms  and  wrists  extended  or  flexed,  the  fingers  clinched  or  flexed  in 
various  ways,  the  legs  and  feet  extended.    This  tonic  stage  lasts  for  fifteen 


FUNCTIONAL   AND   DEGENEKATIVE    DISEASES  477 

or  twenty  seconds;  the  face  becomes  congested  and  then  livid  from  com- 
pression of  the  veins  of  the  neck  and  stoppage  of  respiration.  Gradually 
jerky  movements  of  the  face  and  limbs  begin  and  the  stage  of  clonic  spasm 
sets  in.  The  trunk  and  limbs  are  now  alternately  flexed  and  extended 
with  violent  shock-like  contractions,  the  facial  and  eye-muscles  twitch, 
saliva  collects  in  the  mouth,  and  as  the  tongue  is  often  bitten  it  becomes 
stained  with  blood.  The  movements  are  sometimes  so  violent  that  the 
patient  is  thrown  about  the  bed  or  floor,  and  occasionally  a  limb  is  dis- 
located, usually  the  shoulder.  The  urine  often,  and  the  faeces  occasionally 
are  passed.  The  temperature  is  raised  3^^°  or  1°  F.,  rarely  more.  The 
pulse,  feeble  at  first,  becomes  frequent  and  tense,  and  then,  as  the  attack 
subsides,  becomes  feeble  again.  The  clonic  spasm  lasts  from  one-half 
to  one  or  two  minutes.  It  subsides  gradually,  and  the  patient  sinks  into 
a  stupor,  from  which  he  can  be  roused  with  difficulty.  This  stupor  is 
succeeded  by  a  heavy  sleep  of  several  hours  and  a  feeling  of  hebetude 
which  lasts  all  day.  Vomiting  sometimes  occurs  as  a  terminal  symptom. 
Immediately  after  the  attack  there  is  a  temporary  exhaustive  paralysis, 
with  loss  of  knee-jerk.  The  pupils  contract  again  and  often  oscillate. 
There  may  be  a  slight  amount  of  transient  albuminuria  or  glycosuria. 
The  earthy  phosphates  are  found  increased;  urea  is  not.  There  is  a  dis- 
tinct lessening  of  hsemoglobin  in  the  blood  (Fere)  and  of  hsematoblasts. 
Sometimes  the  attack  is  followed  by  others,  and  for  hours  the  patient 
passes  from  one  convulsion  into  another.  This  condition  is  called  status 
epilepticus.  It  usually  lasts  less  than  twelve  hours,  but  may  last  for  one 
or  more  days  and  until  finally  death  occurs  from  exhaustion.  It  develops 
only  in  the  severer  types. 

Symptoms  of  the  Minor  Attacks. — In  the  minor  attacks  {petit  mat) 
the  patient  suddenly  stops  in  anything  in  which  he  is  engaged,  the 
features  become  fixed,  the  eyes  are  open,  the  face  is  pale,  the  pupils  are 
dilated,  often  slight  twitching  of  the  facial  muscles  or  of  the  limbs  occurs, 
and  consciousness  is  lost.  In  a  few  seconds  the  attack  is  over,  and  the 
patient,  who  does  not  fall,  resumes  his  work  or  conversation,  being 
unconscious  of  what  has  occurred,  except  that  he  has  had  a  "spell." 
Often  there  is  a  warning  sensation  of  aura.  This  is  felt  as  giddiness, 
sense  of  fear,  numb  sensations  of  extremities,  flashes  of  light  or  blind- 
ness, or  choking  sensations.  There  may  be  a  cry  uttered.  The  minor 
attacks  are  in  rarer  cases  accompanied  by  sudden  forced  movements;  the 
patient  runs  a  few  steps;  or  turns  round,  or  makes  some  automatic  move- 
ments. This  is  called  procursive  epilepsy.  Sometimes  the  patient  sud- 
denly falls  to  the  ground,  as  if  the  legs  had  given  way.  He  immediately 
rises  and  is  quite  normal  again.  There  is  no  vertigo  or  apparent  loss  of 
consciousness.     This  is  a  true  "falling  sickness."     Sometimes  he  makes 


478  DISEASES    OF    THE    NERVOUS    SYSTEM 

simply  a  sudden  very  violent  nodding  movement  of  the  head.  This  is 
the  epileptic  "salaam  spasm." 

Symptoms  of  the  Psychical  Attacks. — Sometimes  the  minor  attacks 
are  followed  by  outbursts  of  maniacal  excitement  or  by  sudden  violent 
automatic  movements,  and  in  these  states  the  patient  may  commit 
crimes  of  violence.  In  rare  cases  the  patient  passes  into  a  somnam- 
bulic state,  during  which  he  performs  accustomed  acts,  such  as  driving 
and  walking,  automatically  and  naturally  (somnambulic  epilepsy). 
This  form  of  epilepsy  may  come  on  without  a  preliminary  minor  attack, 
and  then  it  is  to  be  considered  a  ''psychical  epileptic  equivalent." 

Minor  attacks  may  end  in  convulsions  of  a  co-ordinate  type  in  which 
the  patient  jumps,  kicks,  throws  the  arms  about  as  in  hysterical  attacks. 
These  are  called  hysteroid  convulsions. 

The  seizure  may  consist  of  only  a  short  tonic  stage  and  a  few  twitch- 
ings  of  the  limbs,  the  whole  lasting  but  a  few  seconds.  This  is  called  an 
abortive  attack.  Under  the  influence  of  medication,  the  severe  seizures 
are  often  reduced  to  abortive  forms. 

Jacksonian  or  partial  epilepsy  is  a  form  of  the  disease  characterized 
by  convulsive  attacks  affecting  only  a  single  group  of  muscles  or  a  limb, 
and  generally  not  accompanied  by  loss  of  consciousness.  Jacksonian 
epilepsy  is  always  symptomatic  of  some  focal  lesion  affecting  the  cortical 
motor  area  of  the  brain.  This  may  be  a  tumor,  inflammation,  or  injury, 
or  only  some  slight  degenerative  change  in  the  cells  of  the  cortex.  This 
form  of  seizure  is  particularly  significant  of  a  slowly  growing  brain 
tumor  or  syphilis. 

The  epileptic  aura  usually  consists  of  a  sensation  of  numbness,  prick- 
ling or  of  a  breeze  beginning  in  the  hand  or  leg  and  passing  up  to  the 
head  when  consciousness  is  lost.  Still  oftener  there  is  a  peculiar  sensation 
starting  in  the  epigastrium  and  passing  upward.  More  rarely  there  are 
special-sense  aurse,  such  as  a  ball  of  light  in  one  eye,  noises,  or  voices  or 
peculiar  tastes  or  smells.  Besides  these  there  occur  sudden  desire  to  go 
to  stool,  feelings  of  giddiness,  dreamy  states,  peculiar  sensations  in  the 
head,  and  indescribable  general  sensations. 

The  aurse  may  be  divided  into : 

Visceral — -epigastric,  laryngeal,  cardiac,  rectal. 

Cutaneous  sensations. 

Special  senses — flashes  of  light,  etc. 

Psychical — emotions,  dreamy  states,  etc. 

Cephalic — giddiness,  etc. 

The  aura  is  thought  to  indicate  the  seat  of  the  first  discharge  of  nerve 
force,  and  its  study  is  of  most  importance  in  connection  with  sympto- 
matic epilepsies,  as  will  be  shown  later.  The  patient  may  have  only 
the  aura  for  a  long  time  before  the  convulsion  sets  in.     Sometimes  there 


FUNCTIONAL    AND    DEGENERATIVE    DISEASES  479 

never  is  anything  but  the  aura.  This  undeveloped  form  of  epilepsy  I 
have  called  paraepilepsy. 

Frequency  of  the  Attacks. — Epilepsy  with  the  severe  attacks  is  the 
most  frequent  type,  next  come  combinations  of  severe  and  minor  attacks, 
and  next  minor  attacks  alone,  while  the  psychical  forms  are  the  rarest. 
The  severe  attacks  may  come  on  only  once  or  twice  a  year,  and  this 
commonly  occurs  during  the  development  of  the  disease.  The  frequency 
gradually  increases  until  they  occur  every  month,  or  two  or  three  times  a 
month.  Sometimes  the  fits  occur  in  groups  of  four  or  five  every  month 
or  two.  In  very  bad  cases  convulsions  occur  every  day.  The  petit-mal 
attacks  are  more  numerous  and  often  occur  daily. 

Time  of  Attacks. — ^The  moon  and  the  seasons  have  no  influence. 
More  attacks  occur  during  waking  hours  than  during  sleep;  but  two- 
thirds  of  the  attacks  occur  between  8  a.m.  and  9  p.m.  Many  patients 
have  their  attacks  early  in  the  morning  just  after  awakening  {matutinal 
epilepsy).  According  to  Pierce  Clark,  the  hour  in  which  the  greatest 
number  of  attacks  occur  is  9  p.m.,  and  the  fewest  attacks  occur  between 
4  and  7  p.m. 

State  of  Patient  Between  Attacks. — Epileptic  patients  often  feel  better 
for  a  time  after  the  convulsion  is  over.  After  very  severe  attacks  or  a 
series  of  them  there  may  be  a  clouded  consciousness,  amnesia  and  mental 
confusion  for  several  days.  They  not  rarely  suffer  from  severe  neuralgic 
headaches;  the  appetite  is  capricious,  often  in  children  it  is  voracious, 
but  in  older  cases  there  may  be  anorexia;  the  bowels  are  usually  con- 
stipated; the  pulse  is  small,  soft,  and  frequent  in  the  young,  later  it  is 
often  slow.     The  blood  pressure  is  usually  low. 

Mental  Condition. — -A  gradual  mental  deterioration  occurs  in  the 
great  majority  of  epileptics,  but  it  is  slight  in  some  and  not  very  serious 
in  others.  It  shows  itself  by  feebleness  of  memory,  irritability  of  temper, 
selfishness,  incapacity  to  concentrate  the  mind  or  to  carry  out  a  purpose. 
In  children  great  mischievousness  and  lack  of  moral  sense,  with  vicious, 
impulses,  may  appear.  The  mental  deterioration  is  dependent  on  those 
underlying  factors  which  cause  the  disease.  It  is  apparently  associated 
with  the  excessive  number  of  the  fits,  and  the  accompanying  degenerative 
changes  in  the  cortex  of  the  brain.  This  is  not  always  the  case,  nor  is  it 
generally  true  that  deterioration  occurs  more  often  with  petit  mal.  It  is 
more  marked  in  cases  beginning  very  early  in  life,  but  this  is  true  only  when 
there  are  early  and  decided  marks  of  physical  and  mental  degeneration 
present.  A  certain  rather  small  percentage  of  epileptics  become  either 
demented  or  insane.  True  epilepsy  is  rarely  compatible  with  extraordi- 
nary intellectual  endowments.  Caesar,  Napoleon,  Peter  the  Great,  and 
other  geniuses  may  have  had  symptomatic  fits,  but  not  epilepsy. 


480  DISEASES    OF    THE    NEKVOUS    SYSTEM 

Physical  Condition. — Epileptics  are  usually  undersized  and  of  not 
very  robust  constitution  (Fere).  Some  patients,  however,  present  a 
very  vigorous  muscular  development.  They  always  present  some  of 
the  marks  of  degeneration,  physical,  physiological,  or  mental.  Such 
marks  or  stigmata  are  about  ten  times  more  frequent  than  in  healthy 
persons.  The  physical  stigmata  are  (Fere)  short  stature,  cranial  asym- 
metry (in  71  per  cent.),  short  parietal  or  frontal  arc,  and  triangular  skull; 
in  women  high  prominent  forehead ;  bad  teeth  badly  placed,  high  palatal 
arch;  facial  asymmetry;  prominence  of  occiput  and  lemurian  hypophysis; 
differences  in  color,  size,  position  and  shape  of  pupils;  astigmatism  (in 
75  per  cent,  of  cases);  badly  shaped  and  placed  ears;  misplaced  crown  of 
scalp;  low  vital  capacity;  small  genitals,  atrophic  uterus;  greater  develop- 
ment of  left  side;  long  fingers.  Cranial  deformities  of  pronounced  type 
occur  in  epileptics  associated  with  idiocy,  hemiplegia  and  brain  defects 
of  early  origin.  Sometimes,  apparently  from  a  premature  ossification  of 
sutures,  there  are  the  peculiar  shapes  of  the  skull  known  as  scaphocephaly, 
or  steeple  skull,  and  plagiocephaly,  or  obliquely  deformed  skull. 

The  physiological  marks  of  deterioration  are  a  lessened  muscular 
strength  (as  35  to  50),  habit  choreas,  a  rather  imperfect  vision  with  excessive 
amount  of  astigmatism  and  functional  muscular  weakness.  There  is  a 
lessened  vital  capacity,  weak  and  slow  digestion,  often  defective  met- 
abolism and  sexual  atrophy  or  irritability. 

The  psychical  stigmata  are  mental  feebleness,  moral  insensibility, 
a  certain  unreasonableness,  lack  of  insight  and;  irritability.  Some 
have  wayward  and  vicious  impulses,  lack  of  will'  power  and  sexual 
aberrations. 

There  are  cases  of  epilepsy,  however,  in  which  the  mental  powers  are 
fairly  normal  and  continue  well  preserved;  and  I  am  describing  the  non- 
custodial, non-demented  cases.  : 

Association  Diseases. — Epilepsy  may  be  complicated  with  a  de- 
generative myoclonia  (myoclonus  epilepsy).  It  is  sometimes  seen  in 
connection  with  torticollis  and  spasmodic  tic  of  other  types.  Epileptic 
seizures  occur  in  cerebral  syphilis  and  general  paresis. 

Epilepsy  is  regarded  by  some  as  not  a  disease,  but  a  syndrome  or 
symptom-complex  due  to  various  morbid  conditions  of  the  brain.  It  is 
true  that  epilepsy  runs  a  varying  course  and  presents  different  features 
in  different  individuals.  The  grouping  of  cases  in  accordance  with  the 
severity  and  type  of  attack,  the  degree  of  intelligence,  the  tendency  to- 
ward deterioration,  the  physical  and  physiological  defects,  the  tendency 
to  arrest  improvement,  or  increased  severity  of  the  disease  is,  therefore, 
desirable.  Taking  into  account  these  factors,  I  find  in  my  experience  the 
following  general  types  or  groups.  It  is  not  pretended  that  this  is  an 
exact  classification.     Such  a  one  is  not  yet  possible.     It  is  fairly  accurate, 


FUNCTIONAL    AND    DEGENERATIVE    DISEASES  481 

as  I  have  seen  epilepsy  and  I  have  watched  many  cases   for  ten  to 
twenty-five  years. 
The  types  are: 

I.  The  Common  Mixed  Form. — The  attacks  begin  about  puberty. 
They  are  of  haut-  and  petit-mal  type,  but  it  is  the  haut-mal  that  is  trouble- 
some. The  seizures  settle  down  to  four  to  six  monthly  and  occur  singly 
or  in  groups,  by  day  or  night. 

The  patients  have  some  morbid  mental  traits;  they  are  of  moderate 
intelligence  and  this  deteriorates  a  little,  but  does  not  end  in  insanity 
or  dementia.  The  physique  is  fairly  good,  often  robust,  as  to  the 
muscular  system;  there  are  generally  defects  of  physiological  function. 
These  patients  sometimes  get  well  or  get  their  attacks  well  under  control. 

II.  The  Petit-mal  and  Psychic  Type. — The  attacks  are  of  the  psychic 
and  mild  type  alone,  at  least  for  very  many  years.  They  come  on,  as  a 
rule,  in  early  childhood  at  the  fourth  and  fifth  year  or  even  sooner. 
They  increase  until  they  occur  many  times  daily.  The  patients  are 
bright,  often  very  bright  and  precocious  children,  and  they  do  not  de- 
ment as  the  years  go  on,  except  very  late  or  unless  haut-mal  attacks  set 
in.  They  may,  however,  develop  mental  peculiarities  and  defects. 
Physically,  they  are  of  delicate  but  sound  physique.  These  cases  do  not 
get  well.  With  this  petit-mal  type  go  most  of  the  cases  of  cerebral 
automatism,  psychical  epilepsy,  epileptic  sleep  attacks,  etc. 

III.  The  Delayed  Type,  Epilepsia  Tardiva. — ■  The  attacks  do  not 
come  on  until  after  adolescence,  and  sometimes  not  till  the  climac- 
teric. They  are  of  haut-mal  type,  but  petit  mal  is  usually  present  in 
some  degree.  There  is  sometimes  a  history  of  cause,  such  as  infection, 
trauma,  syphilis,  overstrain  and  arterial  sclerosis.  The  attacks  are 
not  very  frequent  relatively,  i.e.,  one  or  two  a  month.  They  are  con- 
trolled fairly  easily,  though  not  entirely.  The  patients  are  of  fair  intel- 
ligence, of  higher  degree  at  least  than  those  of  type  I.  They  do  not 
deteriorate  very  much.  The  epilepsy  of  advanced  years  is  not  of  this 
type,  but  is  a  phase  of  senile  dementia. 

IV.  The  Organic  and  Degenerate  Type. — The  attacks  come  on  in  con- 
nection with  gross  defects  or  disease  or  injuries  of  the  brain.  There  is 
retarded  development,  idiocy,  imbecility,  perversions  and  lack  of  balance 
in  the  mental  functions.  Paralyses,  tics,  etc.,  are  present.  Here  the 
epilepsy  is  only  one  expression  of  the  morbid  cerebral  condition.  The 
cases  are  hopeless,  so  far  as  cure  is  concerned. 

Underlying  all  the  types  there  is,  as  a  cause  of  the  seizure,  some  psychic 
state  or  degenerative  neuron  change.  It  is  very  probable  that  this  change 
is  of  very  much  the  same  character  in  all  cases,  and  that  the  disease  differs 
in  course  and  symptoms  because  the  changes  vary  in  locality,  extent  and 
intensity.     Even  in  idiots  and  paralytics  the  epileptic  phenomena  are 

31 


482  DISEASES    OF    THE    NEKVOUS    SYSTEM 

due  to,  or  associated  with,  this  special  finer  cellular  degeneration,  for  the 
brain  may  be  greatly  injured,  badly  developed,  full  of  cysts  or  tumors  and 
disease,  yet  the  epilepsy  does  not  always  appear. 

V.  Psychogenous  Epilepsy. — ^There  is  a  disease  in  which  the  patient 
suffers  from  apparently  true  epileptic  convulsion,  of  grand-mat  type. 
Psychoanalytic  and  clinical  study,  however,  shows  that  the  convulsions 
are  of  psychic  origin,  due  to  some  irritating  mental  state.  The  convulsion 
is  thought  to  be  the  result  of  this  disturbing  state. 

Pathology. — The  body  of  the  epileptic  shows  sometimes  skin  erup- 
tions and  ulcers,  the  result  of  treatment.  There  are  often  evidences  of 
local  injuries  and  fractures  due  to  falls.  The  organs  may  show  vices 
of  conformation.  The  uterus  is  frequently  infantile  or  sharply  flexed. 
Deformation  of  the  occipital  bone  or  the  atlas  so  as  to  produce  narrow- 
ing of  the  upper  spinal  canal  has  been  noticed.  The  brain  may  be  unduly 
large  or  small,  but  there  is  nothing  constant  in  this,  nor  is  there  an  ab- 
normal difference  in  the  weight  of  the  two  hemispheres.  The  convolu- 
tions show  many  anomalies,  but  there  is  in  them  nothing  specific.  On 
the  whole  the  convolutional  type  is  a  simple  one.  The  pathological 
change  found  in  more  or  less  advanced  epilepsy  is  a  progressive  gliosis 
with  cell  degeneration  in  the  cortex  and  basal  ganglia,  and  the  cornu 
ammonis.  Turner  finds  some  characteristic  changes  in  the  cells  of 
Betz  and  blood-vessels.  In  old  cases  there  is  often  a  chronic  leptomenin- 
gitis, and  vascular  changes  due  to  the  frequent  congestions  of  the  brain 
take  place.  These  consist  in  varicose  and  fusiform  dilatation  of  vessels 
with  evidence  of  small  hemorrhages.  Slight  degenerative  changes  in  the 
nerve-fibres  are  also  observed.  While  cortical  degeneration  and  gliotic 
foci  are  formed  in  epilepsy,  they  are  the  expression  of  some  pathogenic 
state  not  the  cause  of  it. 

The  epileptic  fit  itself  is  a  special  manifestation  of  the  disease  which 
may  be  of  toxic  or  bio-chemical  of  psychic  origin.  It  is  not  likely, 
however,  that  the  psychic  factor  can  do  its  work  on  any  but  a  psy- 
chopathic brain.  It  is  probable  that  in  true  epilepsy  there  is  an  insta- 
bility of  certain  cell  layers  of  the  cortex  cerebri,  and  a  tendency  to 
degenerate.  Whether  this  is  due  to  a  congenital  weakness,  or  the  action 
of  endogenous  poisons,  or  both  we  do  not  yet  know.  The  many  elaborate 
investigations  that  have  been  made  to  ascertain  whether  epilepsy  is 
not  due  to  some  toxic  cause  or  perverted  metabolism  or  endogenous 
ferment,  have  not  established  anything.  Even  in  alcoholic  and  lead 
epilepsy,  the  toxic  agent  is  probably  a  secondary  one. 

The  diagnosis  is  based  on  the  character  of  the  attacks  and  has  to  be 
made  from  hysterical  and  various  toxic  and  symptomatic  convulsions. 

The  aura,  the  scream,  the  quick  loss  of  consciousness,  the  dilated, 
pupils,  the  tonic  convulsion,  the  bitten  tongue,  the  emptied  bladder, 


FUNCTIONAL    AND    DEGENERATIVE    DISEASES  483 

temporary  loss  of  reflexes  are  all  characteristic.  The  hysterical  patient 
sometimes,  but  rarely,  loses  complete  consciousness,  the  epileptic  almost 
always.  Hysterical  patients  do  not  hurt  themselves  in  falling  or  bite 
their  tongue,  and  their  muscular  movements,  while  irregular  and  violent  in 
character,  are  yet  co-ordinate,  i.e.,  they  throw  themselves  about,  kick, 
strike,  etc.  Their  attacks  often  are  produced  by  emotion  and  ended 
by  some  powerful  mental  or  physical  impression.  They  rarely  occur 
in  sleep.  The  slight  rise  of  temperature  in  epileptics  rarely  occurs 
in  hysterics.  Petit  mal  and  epileptic  vertigo  are  distinguished  by  the 
sudden  lapse  of  consciousness  and  by  the  sudden  pallor  and  fixation  of 
the  eyes,  dilatation  of  the  pupils,  and  slight  twitchings  of  the  face. 
Nocturnal  convulsions  are  usually  epileptic. 

Eclampsia,  or  acute  symptomatic  and  refiex  convulsions,  cannot 
always  be  distinguished  from  epilepsy.  The  history  of  the  case,  the 
irregular  and  often  prolonged  character  of  the  fit,  may  enable  one  to 
make  the  diagnosis. 

Course  and  Prognosis. — Epilepsy  shortens  life  to  some  extent; 
most  subjects  do  not  live  beyond  the  age  of  forty  or  fifty.  About 
10  per  cent,  become  demented  or  insane.  Five  or  ten  per  cent,  get 
well.  The  remainder  reach  a  certain  stage  of  severity  in  their  disease 
and  continue  in  it  for  years.  This  severity  depends  on  the  treatment, 
the  nature  of  the  attacks,  and  the  extent  of  degeneration  which  the 
organism  shows.  While  unquestionably  treatment  cures  or  suppresses 
the  disease  in  some  cases,  it  disappears  spontaneously  in  others.  Epilepsy 
developing  after  adolescence  is  not  easily  curable,  but  is  rather  easily 
controlled  and  is  not  so  serious,  except  sometimes  in  old  people.  The 
prognosis  of  petit  mal  is  worse  than  that  of  grand  mal;  that  of  the  two 
combined  is  worse  still,  yet  not  hopeless.  The  psychical  form  of  epilepsy 
is  the  least  amenable  to  treatment.  Epileptic  insanity  and  dementia 
are  incurable.  Death  occurs  rarely  in  the  attacks  except  in  terminal 
stages.     Yet  the  status  epilepticus  is  always  a  source  of  danger. 

Epileptics  who  have  only  a  moderate  number  of  attacks  six  to 
fifteen  yearly,  can  get  along  comfortably  for  years,  doing  their  work 
and  enjoying  a  fair  share  of  the  duties  and  pleasures  of  life. 

Treatment. — The  first  and  essential  rule  of  treatment  is  to  take  cases 
early  and  treat  them  vigorously  from  the  start.  Children  who  have 
had  a  few  convulsions  during  the  first  three  or  five  years  of  life  should 
be  treated  as  if  they  might  develop  epilepsy  between  the  ages  of  ten 
and  fifteen  or  earlier.  The  recurrence  of  a  fit  between  the  ages  of  five 
and  ten  should  excite  apprehension  and  call  for  the  most  diligent  treat- 
ment. Another  rule  is  that  when  epilepsy  is  recognized  in  children  the 
case  should  be  treated  constantly  for  at  least  three  years  after  all  attacks 
have  ceased. 


484  DISEASES    OF    THE    NERVOUS    SYSTEM 

Constitutional  Treatment. — -We  should  use  measures  that  increase 
vasomotor  tone  and  strengthen  and  steady  the  circulation.  Nothing- 
does  this  better  than  water.  Epileptics  should  be  given  showers, 
douches,  cold  sponge  baths,  or  wet  packs  according  to  their  needs  and 
opportunities.  They  should  also  drink  water  freely.  Again,  the  nerv- 
ous system  is  greatly  steadied  and  quieted  by  mental  occupation  that 
interests  one.  Nothing  is  more  unfortunate  than  the  idleness  often 
enforced  on  epileptics.  I  have  seen  the  disease  absolutely  checked  by 
having  a  boy  learn  a  trade  that  he  liked. 

A  second  important  indication  is  diet,  and  the  prevention  of  in- 
testinal decomposition.  In  "petit  mat  particularly  an  absolutely  non- 
irritating  diet,  such  as  milk,  fruit  and  bread,  will  quickly  lessen  or 
stop  the  attacks.  Meats  can  be  taken  in  moderation  if  eaten  slowly. 
As  a  rule  it  is  a  little  safer  to  keep  meat  out  of  children's  diet  for  a  time; 
but  in  adults  it  is  not  necessary,  though  it  should  be  given  in  moderation. 
A  practically  salt-free  diet  is  advisable  part  of  the  time. 

Removal  of  Irritating  Causes.  The  rheumatic,  gouty,  and  so-called 
tuberculous  diatheses  do  not  stand  in  any  close  relation  to  epilepsy. 
The  condition  known  as  lithsemia,  however,  in  which  there  are  insuf- 
ficient oxidation  and  excretion  of  products  of  tissue  waste,  needs  atten- 
tion. Hence  the  use  of  bicarbonate  of  potassium,  salicylate  of  sodium, 
the  alkaline  mineral  waters,  and  a  restricted  diet  are  not  rarely  indicated. 

The  importance  of  reflex  irritations  has  been  much  over-estimated. 
Still  they  must  be  considered.  The  most  serious  are  those  arising  from 
the  gastro-intestinal  tract,  the  sexual  organs  and  the  eyes.  Phimosis 
if  present  must  be  relieved,  and  masturbation  or  sexual  excesses  stopped, 
if  possible.  It  is  admitted  now  that  removal  of  the  ovaries,  even  if 
diseased,  never  cures  true  epilepsy,  though  it  may  help  hysterical 
convulsions. 

Astigmatism  and  hypermetropia  should  be  corrected;  also  ocular 
insufficiencies  if  these  are  pronounced. 

Proper  attention  to  the  frequent  constipation  and  dyspepsia  is  of 
course  necessary. 

Specific  Treatment. — ^Physicians  who  undertake  the  treatment  of 
epileptics  often  do  not  realize  the  seriousness  of  their  responsibilities. 
Many,  I  fear,  simply  give  a  little  bromide,  stop  the  meat,  circumcise 
the  boy,  and  say  they  think  the  child  will  outgrow  it.  But  children  do 
not  outgrow  it;  they  steadily  get  worse  unless  something  definite  is 
done,  and  well  done  for  a  long  time.  With  proper,  prompt,  and  pro- 
longed treatment,  the  attacks  can  be  entirely  controlled  in  5  to  10  per 
cent,  of  cases,  and  I  believe  more.  They  can  be  greatly  controlled  in 
over  one-half  the  cases,  so  that  the  patient  may  be  able  to  continue  his 
education  and  do  some  work  in  life.     But  this  cannot  be  accomplished 


FUNCTIONAL    AND    DEGENERATIVE    DISEASES  485 

by  any  casual  dosing  or  occasional  consultation  with  some  high  authority. 
The  physician  should  approach  the  responsibility  of  a  case  of  epilepsy 
as  he  would  that  of  a  mortal  surgical  condition,  in  which  much  depends 
on  knowledge  and  attention  to  all  the  details  of  a  long  technic. 

It  is  conceded  that  the  colony  treatment  of  epilepsy  is  the  one  which 
approaches  most  nearly  the  ideal  in  effectiveness,  but  it  cannot  be 
applied  to  all  classes — at  least,  for  a  long  time — and  perhaps  never  to 
a  certain  rather  large  percentage.  There  must  always,  therefore,  be  a 
good  many  epileptics  who  have  to  be  treated  at  their  homes,  and  whose 
care  must  be  directed  by  the  family  physician  or  the  specialist. 

For  this  class  of  persons  I  have  gradually  evolved  a  somewhat 
specific  treatment  of  epilepsy,  which  seems  to  produce  the  most  satis- 
factory results  in  those  cases  in  which  a  reasonable  opportunity  for 
therapeutic  effort  exists.  That  is  to  say,  cases  wdiich  are  not  of  verj^ 
long  standing,  and  which  have  not  already  undergone  serious  mental 
deterioration,  and  cases  in  which  the  mental  and  physical  degenera- 
tion, at  the  beginning,  is  not  of  a  very  high  grade. 

The  features  upon  which  emphasis  must  be  laid,  in  the  treatment 
of  epilepsy,  are: 

First,  the  fact  that  the  course  of  treatment  about  to  be  instituted 
is  to  last  for  at  least  two  j^ears,  and  that  all  measures  prescribed  must 
be  carried  out  with  the  greatest  fidelity  and  exactness  during  that 
time,  no  matter  how  well  the  patient  may  seem,  or  how  unnecessary 
regimen  and  drugs  may  appear  to  be.  The  preparation  and  outlining 
of  treatment  should  receive  the  care  and  attention  such  as  is  given  to  a 
capital  operation. 

Second,  the  use  of  the  pure  bromide  of  sodium  or  some  other  salt 
(there  is  no  special  merit  in  mixed  bromides)  in  combination  with  the 
glycero-phosphate  of  soda  or  of  soda  and  lime  so  that  a  patient  takes  on 
an  average  60  grains  of  the  bromide  of  soda  and  20  to  30  grains  of  the 
phosphate,  in  twenty-four  hours.  To  this  combination  iron  and  a  little 
arsenic  may  be  added  at  times.  By  the  combination  of  proper  soluble 
phosphates  with  bromide  and  ehminative  measures,  the  depressing 
effect  of  the  bromide  can  be  greatly  lessened  and  the  patient  can  continue 
bright  and  active  under  a  fairly  large  dose  of  the  drug.  This  has  been 
tested  by  me  now  for  fifteen  years,  mainly  in  private  practice,  but  also 
in  dispensary  work.  The  maximum  dose  of  bromide  which  can  be  taken 
in  this  combination  is  sometimes  as  high  as  90  grains  a  day,  but  rarely 
more,  and  not  often  as  much.  The  phosphate  should  occasionally  be 
omitted,  and  the  form  changed.  Certain  patients  cannot  take  bromides, 
however,  and  are  not  benefited  by  them  in  any  way. 

Third,  I  have  found  it  often  an  efficacious  plan  in  treatment  to  in- 
termit the  medication  for  either  one  or  two  days  in  each  seven.     During 


486  DISEASES    OF    THE    NERVOUS    SYSTEM 

these  days,  e.g.,  a  Wednesday  and  Sunday,  the  drug  is  stopped,  and 
in  its  place  is  given,  three  times  a  day,  before  meals,  a  tumbler  of  hot 
water,  and  with  it  an  alkaline  laxative.  The  ordinary  tablet  of  rhu- 
barb and  soda,  with  nux  vomica,  usually  answers  this  purpose.  Some- 
times 20  grains  of  bicarbonate  of  soda  are  enough.  Its  purpose  is  to 
flush  out  the  stomach  and  bowel  and  cleanse  the  gastro  -intestinal  canal 
twice  a  week,  thus  preventing  the  accumulation  of  drugs  and  toxins. 
After  meals  on  these  days  I  sometimes  give  10  drops  of  tincture  of  iron 
or  some  needed  tonic.  I  have  not  seen  any  access  of  convulsion  during 
the  day  or  the  day  after  such  intermission.  With  this  stomach  treat- 
ment there  should  be  in  many  cases  a  colon  irrigation  using  a  hot  high 
bicarbonate  of  soda  solution.  This  is  given  about  once  a  week.  Some- 
times in  its  place  I  use  an  injection  of  a  pint  of  warm  sweet  oil  at  night 
followed  by  a  simple  enema  in  the  morning. 

Fourth,  an  important  measure  which  I  employ  in  the  treatment  is 
the  securing  of  active  physical  exercises  for  about  twenty  or  thirty 
minutes,  at  least,  three  times  a  week.  This  must  be  done  either  by 
some  active  sport,  like  boxing,  by  exercises  in  the  gymnasium,  by 
tennis,  skating,  or  by  the  simpler  methods  of  chopping  or  sawing  wood 
skipping  the  rope,  dancing,  or  punching  the  bag;  but  the  exercises  of 
whatever  kind  should  be  short  and  to  the  point  of  free  perspiration. 
After  this  exercise,  the  patient  is  given  a  cool  bath.  Delicate  persons, 
women,  and  those  who  are  unable  to  carry  out  such  exertion,  I  direct  to 
purchase  a  "hot-box"  and  take  a  hot-box  sweat,  followed  by  a  cool  bath, 
three  times  a  week.  These  boxes  are  not  expensive,  and  can  be  set  up 
with  little  trouble. 

Fifth,  the  question  of  diet  is  attended  to,  as  indicated  above. 
The  medication  should  be  increased  rather  than  diminished  as  the 
patient  gets  better;  he  should  take  more,  if  possible,  at  the  end  of  the 
second  year  than  at  the  beginning  of  the  first,  if  the  attacks  are  controlled. 
After  four  years  one  can  feel  safe,  not  before.  There  are  few  other 
drugs  of  any  importance  in  epilepsy,  though  freak  cures  happen  under 
all  kinds  of  measures.  Tincture  of  simulo  seems  to  have  some  value 
in  doses  of  5i-  ter  in  die  upward.  Atropine  in  very  large  doses  (gr.  3^^o 
to  j-^s)  gradually  increased  sometimes  helps  petit-mal  types  strikingly. 
Veronal  and  luminal  may  sometimes  be  given  in  cases  in  which  bromides 
have  no  effect,  or  to  aid  their  effects. 

There  are  some  cases  in  which  a  glandular  defect  exists,  hypothy- 
roidism being  the  most  frequent  in  my  experience.  Small  doses  of 
thyroid,  gr.  3^  to  gr.  ii.,  may  be  indirectly  helpful.  The  other  glands 
may  be  used  as  indicated.     They  only  act  as  adjuncts. 

Growing  children  must,  as  a  rule,  be  taken  from  school.  This  is  un- 
fortunate, but  it  seems  indisputably  necessary.    The  education,  however, 


FUNCTIONAL   AND    DEGENERATIVE   DISEASES  487 

should  be  allowed  to  proceed  and  regular  fixed  short  hours  of  study  be 
given.  The  child  should  be  allowed  to  live  as  nearly  a  normal  life  as 
possible.  If  old  enough,  some  can  be  taught  a  trade  or  some  handi- 
craft with  advantage.  The  grown  person  should  be  urged  to  adopt  or 
continue  in  some  occupation,  of  which  an  out-door  one  is  preferable,  but 
any  occupation  is  preferable  to  idleness. 

The  most  difficult  cases  after  the  degenerates  and  those  with  organic 
brain  disease  are  the  bright,  precocious  children  who  develop  yetit  rnal 
alone  and  who  have  daily  attacks.  They  are  usually  not  amenable 
to  bromide  medication  in  any  form.  After  a  thorough  trial  of  this, 
however,  even  to  the  point  of  bromidation,  and  using  every  possible 
tonic  and  eliminant,  the  patient  is  best  left  to  hygienic  measures  alone. 

This  treatment  of  epilepsy  always  presupposes  a  preliminary  elimina- 
tion of  all  reflex  causes.  If  the  epilepsy  is  local  {i.e.,  Jacksonian)  or 
even  if  it  began  as  a  local  affair,  it  is  advisable  to  operate,  and  if  any 
source  of  irritation  is  seen  in  the  cortex  it  should  be  removed.  Oc- 
casionally this  does  good,  but  not  always.  Often  epileptics  are  brought 
to  us  with  scars  on  the  scalp  and  a  history  of  some  old  injury,  perhaps 
even  of  fracture.  If  the  epilepsy  is  general,  however,  and  does  not  seem 
to  have  started  from  the  injured  zone,  operations  are  of  no  use. 

It  goes  without  saying  that  there  are  many  epileptics  who  are  too 
advanced  in  the  disease  or  too  degenerate  for  treatment  and  who  need 
only  custodial  measures. 


CHAPTER  XXI 

THE  PSYCHO -NEUROSES 

CONSTITUTIONAL  INFERIORITY,  HYSTERIA  AND  ALLIED  STATES, 

PHYCHASTHENIA 

Introduction. — The  term  psycho-neurosis  is  given  to  a  number  of  dis- 
orders in  which  the  nervous  symptoms  are  in  the  main  dominated  or 
caused  by  the  mental  state.  This  mental  state  is  a  morbid  one,  but  is 
not  of  sufficient  degree  to  call  for  custodial  care  or  justify  applying  to  it 
the  term  insanity.     It  is  just  a  minor  psychosis. 

There  is  a  difference  of  view,  as  to  the  grouping  of  the  psycho-neuroses. 
One  has  to  follow  some  practical  method,  and  I  include  under  this  term; 
(1)  The  psychopathic  diathesis  or  constitutional  inferiority.  (2) 
Hysteria  and  allied  states.  (3)  Psychasthenia.  (4)  Certain  mild  and 
abortive  forms  of  the  major  psychoses. 

The  study  of  the  pathogenesis  of  the  psycho-neuroses  takes  one  into 
difficult  and  unsettled  fields,  but  the  situation  as  between  clinical  and 
dynamic  neurology  may  be  stated  as  follows: 

The  clinician  finds  that  an  apparently  healthy  person  has  gradually 
or  suddenly  developed  an  automatic  state,  a  fixed  idea,  or  a  functional 
paralysis.  He  inquires  into  the  causes  and  finds  (a)  a  nervous 
heredity  (e.g.,  the  father  alcoholic,  the  mother  tuberculous) ;  (6)  the 
patient  herself  of  nervous  type  and  (c)  a  sufferer  from  an  emotional  strain 
or  shock  followed  by  the  psycho-neurosis,  (d)  He  learns  the  patient's 
mental  make-up  and  intellectual  equipment,  the  temperament  and  the 
bodily  condition. 

The  data  gained  under  a,  b,  c,  d,  tell  him  the  cause  of  the  disorder  and 
show  along  what  lines  to  work  for  cure.  This  is  descriptive  or  clinical 
neurology. 

But  the  dynamic  neurologist  goes  further  and  searches  into  the  intimate 
mental  mechanism  of  the  process  by  which  the  mind  became  thus  mor- 
bidly changed.  This  mechanism  according  to  some  consists  in  a  blocking 
of  association  processes  and  a  limiting  and  re-grouping  of  neural  units. 

Thus  the  phenomenon  of  double  personality,  hypnotism,  hysterical 
crises,  trance,  are  explained,  if  it  is  an  explanation,  by  supposing  that  there 
is  a  break  and  re-grouping  of  the  association- work  of  the  brain.  Ordi- 
narily the  associations  aroused  by  the  stimuli  of  thought,  emotion  or  sense 
have  free  play  in  accordance  with  what  the  individual's  environment  and 
training  have  developed.     If  he  is  hypnotized  or  obsessed  this  free  play 

48S 


THE    PSYCHO-NEUROSES  489 

of  association  does  not  take  place.  The  patient  hears  and  sees  and  thinks 
only  what  is  suggested  to  him,  by  the  hypnotizer  or  by  his  dominating 
idea.  All  his  mental  activity  is  along  a  particular  group  of  associations. 
At  the  synapses  of  the  nerve  cells,  there  is  a  blocking  off  of  the  ordinary 
to-and-fro  play  of  the  neural  currents.  This  same  process  occurs  when 
the  personality  becomes  changed.  One  neural  unit  of  association  ac- 
tivities underlies  the  personality  of  Mr.  Hyde  and  another  group  those 
of  Dr.  Jekyl.  This  is  the  mechanism  of  trance-states  of  cerebral  auto- 
matism, and  even  of  absent-mindedness  and  intense  attention.  It  may 
be  applied  to  the  explanation  of  an  uncontrollable  and  consciously  foolish 
fear  or  a  hysterical  paralysis. 

We  do  not  know  the  exact  psychic  or  physiological  process  by  which 
this  blocking,  and  re-grouping  of  associations  takes  place.  It  is  done  by 
effort  of  the  will,  by  fatiguing  the  attention,  by  the  action  of  powerful 
emotion,  by  endogenous  ferments  perhaps,  and  by  chemical  poisons. 

Whether  the  Freudian  school  accepts  the  dissociation  theory  I  do  not 
know,  and  it  is  difficult  to  find  out.  But  if  so  it  would  be  only  a  detail 
in  their  explanation  of  the  mechanism  of  these  same  phenomena.  With 
this  school  the  forces  of  the  subconscious  would  be  the  agent,  which  in 
struggling  to  fulfil  desire  caused  blocking  of  the  synapses,  neural  dis- 
sociations and  the  phenomena  of  altered  personality,  of  hysteria  and 
trance. 

The  Freudian  school  finds  that  the  subconscious  mind  is  the  re- 
pository of  a  libido  or  desire  whose  urgings  have  been  with  varying  success 
repressed  and  forgotten.  Here  are  stored  up  the  memories  and  instinctive 
trends  of  infancy,  the  emotional  shocks  and  painful  experiences  of  child- 
hood. Though  repressed  and  pushed  back  into  the  subconscious,  yet 
they  still  exist  as  potent  ''complexes"  and  may  be  a  source  of  trouble- 
some mental  states  and  bodily  symptoms.  The  libido,  unable  to  force 
itself  into  consciousness  and  express  itself  in  the  normal  infantile  way 
takes  devious  paths  of  activity  and  produces  its  obsessions,  paralyses, 
etc.,  in  trying  to  secure  satisfaction.  This  is  shown  through  psycho- 
analysis, by  studying  dreams  and  by  various  other  diagnostic  methods. 
The  result  leads  to  the  view  that  the  changed  personality,  the  spasm, 
the  anaesthesia,  the  paralysis,  the  exhaustion  are  the  expressions  of  a 
suppressed  wish. 

This  psychic  mechanism  offers  a  satisfactory  explanation  to  some.  It 
is  a  poetical,  but  not  an  adequate,  practical  or  always  safe  method  for  the 
practising  neurologist. 

For  to  him  as  a  clinician  the  causes  leading  to  instability,  obsession, 
the  dominance  of  fear  are  not  altogether  or  mainly  subconscious.  In 
most  the  influences  of  heredity,  of  a  constitutionally  weak  brain,  of 
physical  disease,  of  obvious  and  conscious  suffering,  of  maladjustments. 


490  DISEASES    OF    THE    NERVOUS    SYSTEM 

poor  insight  and  defective  education  are  the  vitally  important  things,  often 
not  easily  recognized  but  obviously  to  be  treated.  The  subconscious 
psychic  factor  is  certainly  often  only  an  extra  and  minor  element.  It 
is  the  final  slight  impact  which  makes  an  unstable  structure  fall.  Often 
it  is  not  subconscious  really,  and  if  present  has  only  an  academic  and 
metaphysical  importance. 

Hence,  I  believe  in  treating  the  psycho-neuroses,  by  correcting  the 
general  instability,  educating  the  inferiorly  developed,  removing  irrita- 
tions, and  trying  to  make  a  perhaps  rather  poor  human  system  carry  its 
proper  load. 

True  psycho-therapeutics  is  really  a  form  of  education  or  re-education. 
It  belongs  to  no  school,  but  is  part  of  ancient  medical  art  and  physicians 
have  known,  and  more  or  less  applied,  the  method  for  centuries. 

CONSTITUTIONAL  INFERIORITY.      PSYCHOPATHIC  DIATHESIS 

This  is  a  term  applied  to  a  condition  characterized  by  a  congenitally 
unstable,  nervous  system,  and  more  particularly  an  unstable  mental 
condition.  The  patients,  however,  as  a  rule,  are  sufficiently  under 
control  of  themselves  and  their  morbid  tendencies,  to  be  responsible 
or  partially  responsible  for  their  acts. 

It  includes  persons  who  suffer  from  "nervousness,"  constitutional 
despondency  and  constitutional  excitement  and  morbid  instincts. 

While  constitutional  inferiority  may  exist  without  developing  any 
well-marked  neurosis  or  psychosis,  some  episodical  outbreaks  often 
occur. 

When  the  trouble  is  more  especially  associated  with  weakness  of  will, 
feebleness  of  mind,  incapacity  to  decide  or  inhibit,  or  to  initiate,  it  is  in 
particular  a  quantitative  inferiority.  When  the  mind  is  not  retarded  or 
intellectually  defective,  but  is  dominated  by  morbid  instincts  (sexual  or 
criminal)  or  unsocial  trends,  the  person  is  more  particularly  a  case  of 
qualitative  inferiority  and  he  is  then  sometimes  called  a  psychopathic 
personality.     Various  major  psychoses  may  develop  on  this  soil. 

Constitutional  inferiority  exists  as  an  independent  state  but  it  may 
underlie  the  following  conditions: 

Neurasthenia. 

Psychasthenia. 

Hysteria. 

Hypchondria. 

Dipsomania. 

Compulsive  and  impulsive  psychoses. 

Persons  with  a  constitutional  inferiority  may,  under  proper  environ- 
ment and  educational  guides,  live  fairly  normal  and  useful  lives.     If, 


THE    PSYCHO-NEUROSES  491 

however,  they  are  brought  up  in  such  a  way  as  to  allow  indulgence  in 
abnormal  impulses  or  habits;  if  they  thus  acquire  vicious  modes  of  living 
or  go  to  excesses  in  any  direction,  they  may  develop  criminality  or 
some  of  the  formal  types  of  insanity,  such  as  paranoia  or  even  dementing 
types  of  insanity,  like  dementia  praecox. 

It  is  often  somewhat  difficult  to  say  whether  a  person  is  simply  a 
psychopathic  personality,  or  whether  he  has  not  a  constitutional  inferiority 
in  which  criminal  tendencies  have  been  allowed  to  develop.  It  is  often 
possible  by  the  force  of  teaching  and  the  influences  of  environment, 
to  change  the  morbid  tendencies,  so  that  an  inferior  or  psychopathic 
personality  may  become  a  fairly  useful  man.  Great  care  should,  there- 
fore, be  exercised  in  applying  to  a  patient  the  term  "constitutional 
inferiority"  to  excuse  criminality,  since  there  may  have  been  only  a  slight 
tendency  which  has  grown  through  indulgence. 

HYSTERIA 

Hysteria  has  been  defined  as  the  expression  of  a  symbolic  conversion 
of  psychic  into  physical  states.  This  condition  in  which  the  psychical 
is  converted  into  physical  is  said  by  followers  of  the  Freudian  School  to 
be  an  index  of  the  aspirations  of  the  race.  For  the  manifestations  of  hys- 
teria are  thought  to  be  the  expression  of  subconscious  instincts  or  desires. 

Such  a  view  need  not  interfere  with  a  pragmatic  method  of  dealing  with 
the  subject  such  as  I  adopt  in  the  following  description,  in  which  the 
mental  traits  of  the  hysterical,  and  the  physical  phenomena  they  show 
are  presented  in  clinical  narrative  without  forcing  into  them  philosophical 
and  questionable  mechanistic  interpretations. 

Hysteria  is  in  its  broadest  sense  not  a  specific  disease  but  a  morbid 
biological  reaction,  in  which  morbid  bodily  disturbances  are  caused 
by  more  or  less  subconscious  mental  states. 

Hysteria  is  a  widely  prevalent  quality  of  the  human  character. 
It  displays  itself  in  brief  and  often  trivial  episodes,  such  as  unreasonable 
emotional  explosions  of  crying  and  laughing,  and  in  motor  and  visceral 
crises.  These  are  often  to  be  considered  only  as  symptoms  of  a  natural 
instability,  and  they  are  often  associated  with  other  real  and  organically 
morbid  conditions.  When  this  reaction  is  very  severe,  persistent  and 
disorganizing,  we  have  major  hysteria,  which  is  distinctly  a  disease  or 
fixed  symptom-group  having  a  definite  origin,  course  and  symptoms. 

A  slight  degree  of  this  hysterical  reaction  is  very  common  and  can 
hardly  be  called  abnormal.  Nearly  all  women  are  said  to  be  somewhat 
hysterical. 

When  the  condition  occurs  occasionally  and  under  stress  of  emotion, 
it  is  episodical  or  minor  hysteria. 


492  DISEASES    OF    THE    NERVOUS    SYSTEM 

Etiology. — Of  the  predisposing  causes  of  hysteria  in  general,  heredity 
is  the  most  important.  In  about  75  per  cent,  there  is  a  history 
of  hysteria,  or  some  neurosis  or  psychosis  in  the  parents.  The  disease 
is  transmitted  more  often  by  the  mother.  Heredity  is  particularly 
apt  to  be  important  in  the  hysteria  of  children;  it  is  a  much  smaller 
factor  in  hysteria  of  adult  males.  Hysteria  is  a  disease  of  early  adult 
life,  most  cases  occurring  between  the  ages  of  from  fifteen  to  twenty- 
five  in  females;  it  occurs  later  in  males.  Hysteria  attacks  children 
between  the  ages  of  eight  and  fifteen,  chiefly  between  eleven  and 
fourteen.  The  trouble  affects  women  more  than  men  in  the  propor- 
tion of  four  to  one,  varying  much  with  race,  climate  and  occupation. 
Hysteria  major,  however,  occurs  oftener  in  men  than  women;  it 
occurs  in  adult  and  middle  life  and  there  is  often  no  hereditary  history. 
These  statements  are  based  on  personal  experience  of  this  type  of 
hysteria  as  seen  in  this  country.  They  do  not  correspond  with  the 
observations  of  European  observers  or  of  alienists,  but  are  certainly  true 
for  the  type  of  disease  which  I  am  describing.  Hysteria  occurs  in  all 
classes  of  life,  but  rather  less  frequently  in  the  middle  classes  than 
among  the  poor  and  the  very  rich.  Male  hysteria  is  more  frequent  in 
the  poorer  classes  who  are  subjected  to  the  influences  of  alcoholism, 
poverty,  injuries,  etc.  Hysteria  is  certainly  much  less  frequent  in 
its  severer  forms  in  this  country  than  in  some  parts  of  Europe,  par- 
ticularly France.  In  my  experience  it  is  much  less  frequent  than  epilepsy 
in  the  northern  and  eastern  parts  of  this  country.  It  occurs,  how- 
ever, quite  frequently  in  the  negroes  and  also  in  the  Latin  races  of  this 
country.  Bad  methods  of  education  and  bad  sexual  habits  undoubtedly 
tend  to  promote  the  development  of  the  disease. 

The  most  important  single  exciting  factor  is  powerful  emotion, 
particularly  fear.  Other  emotions  of  an  allied  character — excitement, 
sorrow,  anxiety — may  bring  on  attacks.  The  disease  can  be  developed 
by  imitation.  Injuries  combined  usually  with  mental  shock  are  fruit- 
ful causes  of  producing  hysteria.  The  infectious  fevers,  syphilis,  diffuse 
hemorrhages,  the  poisons — -lead,  mercury,  and  tobacco — the  adminis- 
tration of  ether,  mental  and  bodily  and  sexual  excesses,  are  all  important 
agents  in  developing  the  disease.  Acute  alcoholism  is  not  very  rarely 
followed  by  hysteria. 

General  Symptoms. — Mental. — Mental  hysteria  shows  itself  clinically 
in  certain  morbid  moral  manifestations.  The  typical  moral  hysteric, 
for  example,  is  intensely  self-centred,  craves  for  sympathy  and  is 
desirous  of  being  always  in  the  centre  of  the  stage.  To  secure  her  ends 
she  exaggerates  symptoms,  tells  lies,  practises  cunning  deceits  and 
constructs  false  and  ingenious  stories.  Such  patients,  in  order  to  gain 
their  end  and  excite  human  sympathy,  will  even  injure  and  mutilate 


THE    PSYCHO-NEUROSES  493 

themselves  or  will  prevent  the  healing  of  their  wounds.  In  fact,  all 
manner  of  devices  are  used  to  make  it  appear  that  they  have  some  ailment 
or  painful  condition  which  demands  continual  attention.  Without  her 
headache,  or  exhaustion,  or  neuralgia,  the  hysterical  woman  knows,  or 
her  subconsciousness  knows,  she  would  not  count  in  the  household  for 
more  than  she  is  worth  there. 

Aside  from  the  peculiarities  of  the  hysterical  mind  along  the  moral 
lines,  the  hysterical  person  develops  other  characteristic  mental  phe- 
nomena. These  consist  of  dreamy  states,  periods  of  amnesia  and  auto- 
matism and  also  disorders  of  mentality  which  go  by  the  name  of  hysterical 
insanity. 

The  great  proportion  of  patients  who  have  disturbances  of  bodily 
function  such  as  paralyses,  anaesthesias,  neuralgias,  may  be  practically 
free  from  the  exaggerated  form  of  moral  hysteria,  and  appear  only  perhaps 
rather  dull  and  depressed,  nervous  and  apprehensive. 

Physical. — The  varioua:.forms  in  which  the  somatic  phases  of  hysteria 
show  themselves  may  be  grouped  as  follows: 

Convulsions;  tremors;  clonic  and  tonic  spasms,  paralyses  of  the  type 
of  monoplegia,  hemiplegia  and  paraplegia;  neuralgias  and  anaesthesias. 

There  are  also  vasomotor  and  secretory  disturbances;  and  disturb- 
ances of  the  autonomic  system  shown  in  vago-tonic  and  sympathetico- 
tonic  attacks. 

The  reflexes  are  to  some  extent  disturbed. 

Special  Types. — Hysteria  minor  or  the  hysterical  temperament  is 
characterized  by  an  interparoxysmal  condition  of  emotional  weakness, 
nervousness,  hypersesthesia  and  pains,  and  by  crises  of  an  emotional, 
motor,  sensory  or  visceral  type.  In  hysteria  minor  there  are  no  perma- 
nent objective  marks  like  anaesthesia  and  paralysis,  and  rarely  convulsive 
seizures.  The  patient,  who  is  almost  always  a  girl  or  young  woman, 
gradually  develops  an  undue  sensitiveness,  the  mind  is  depressed,  and 
she  gets  easily  alarmed.  She  has  feelings  of  nervousness  and  lacks  con- 
trol over  the  emotions,  she  laughs  and  cries  very  easily  and  yields  to 
every  impulse.  She  suffers  from  headaches,  which  are  usually  diffuse 
and  often  severe  and  chronic,  and  from  spinal  pains.  She  sleeps,  as  a 
rule,  rather  badly  and  often  has  disagreeable  dreams.  She  has,  under 
any  little  excitement,  sensations  of  tickling,  fullness  or  choking  in  the 
throat,  forming  the  condition  known  as  globus.  Excitement  also  brings 
on  attacks  of  trembling  or  chilly  feelings  which  come  and  go.  There  is 
more  rarely  a  considerable  amount  of  vasomotor  instability,  as  shown  by 
flushings  and  by  coldness  of  the  extremities,  and  vago-tonic  attacks. 

She  has  with  more  or  less  frequency  distinct  crises  of  an  emotional 
character,  during  which  she  laughs  or  cries  without  apparent  cause,  or 
at  least  to  an  extent  beyond  her  control.     She  may  have  attacks  of 


494  DISEASES    OF   THE    NERVOUS    SYSTEM 

vomiting  or  headache,  or  of  intense  mental  excitement  amounting  almost 
to  delirium.  In  some  cases  the  patient  has  somnambulic  attacks  at 
night,  or  she  may  have  under  a  little  excitement  attacks  of  cerebral 
automatism  during  which  she  involuntarily  does  things  that  she  is  entirely 
unconscious  of  when  she  comes  out  of  the  attack.  The  crises  are  fol- 
lowed by  a  copious  discharge  of  very  light  urine. 

With  all  these  symptoms  there  may  be  the  moral  traits  above  described. 

Hysteria  major  is  characterized  by  interparoxysmal  manifestations 
of  anaesthesia,  paralyses,  contractures,  tremors,  peculiar  mental  condi- 
tions, and  by  paroxysms  of  an  emotional,  convulsive,  or  other  serious 
nature.  Hysteria  major  is  what  is  usually  meant  when  one  speaks  of 
hysteria  as  a  disease;  it  includes  also  hystero-epilepsy.  The  onset  may 
be  gradual,  but  not  infrequently  it  follows  some  shock,  the  first  symptom 
being  a  convulsion,  a  paralysis,  or  some  emotional  outburst. 

The  crises  of  hysteria  may  be:  Psychical;  motorial;  sensory;  visceral; 
angio-neurotic. 

The  most  common  of  the  paroxysms  of  hysteria  are  emotional 
outbursts  of  crying  or  laughing;  after  this  come  motor  disturbances  in 
the  shape  of  convulsions  of  various  types  or  of  hemiplegia  or  other  form 
of  paralysis.  Besides  this  we  have  attacks  of  severe  pain,  forming 
neuralgic  crises;  attacks  of  nausea,  gastralgia  and  vomiting,  forming 
gastric  crises;  much  more  rarely  there  are  prolonged  attacks  of  hysterical 
coughing,  hiccoughing,  sneezing,  or  rapid  breathing.  The  hysterical 
seizure  may  also  take  the  form  of  attacks  of  trance  and  lethargy,  catalepsy 
amnesia,  and  cerebral  automatism. 

The  emotional  crises  are  episodes  of  the  same  nature  as  occur  in 
minor  hysteria. 

Hysterical  convulsions  have  two  rather  well-defined  types.  One 
of  them  is  the  ordinary  form  of  hysterical  convulsions;  the  other  is  a 
much  more  severe  disturbance  in  every  way  and  is  known  as  a  hystero- 
epileptic  or  hysteroid  attack.  In  the  hysterical  convulsion  the  patient, 
under  the  influence  of  some  excitement,  injury,  or  acute  gastric  disturb- 
ance, rather  suddenly  falls  down  and  begins  to  go  through  various 
irregular  movements  of  the,  body,  such  as  thrashing  with  the  arms,  kick- 
ing with  the  legs,  throwing  the  head  from  side  to  side,  rolling  about  on  the 
bed  or  floor.  In  the  more  distinctly  convulsive  seizure  the  hands  and 
arms  and  fingers  are  flexed,  the  legs  and  feet  are  extended,  the  eyes  are 
generally  closed,  the  eye-balls  often  converged  or  moved  about  irregu- 
larly, the  pupils  dilated.  There  is  some  lessening  of  sensation  over  the 
body  and  of  the  conjunctivae.  The  patient  often  utters  noises  or  screams 
at  intervals.  She  may  bite  her  lips,  but  does  not  bite  the  tongue,  nor 
does  she  ever  hurt  herself  in  her  various  contortions.  The  attack  may 
last  for  half  an  hour  to  several  hours,  unless  some  measures  are  taken 


THE    PSYCHO-NEUROSES  495 

to  break  it  up.  In  other  forms  of  hysterical  convulsion  there  is  simply 
a  general  shaking  or  trepidation  of  the  body  as  though  the  patient  had 
a  chill;  in  other  cases  again  the  main  type  of  movement  is  that  of  opis- 
thotonos, the  patient  rising  up  upon  the  head  and  heels  and  arching  the 
body  in  as  tetanus.  Again  the  attack  may  consist  simply  of  a  little 
rigidity  of  the  body  or  of  a  series  of  rhythmical  movements  of  the  head 
or  trunk  or  limbs,  the  patient  sitting  up  and  oscillating  the  head  or  sway- 
ing the  trunk  or  moving  the  arms,  uttering  at  the  same  time  incoherent 
words.  In  still  other  cases  the  patient  simply  falls  down  and  lies  un- 
conscious, like  a  person  sleeping,  for  a  few  minutes  or  even  an  hour.  In 
children  the  attacks  may  be  associated  with  peculiar  noises  and  move- 
ments in  imitation  of  animals,  such  as  the  growling  of  a  dog  or  the  mew- 
ing of  a  cat.  This  condition  is  called  therio-mimicry.  In  some  instances 
the  attack  may  be  accompanied  by  or  may  end  in  a  condition  of  mental 
excitement  approaching  delirium.  The  patients  while  suffering  from  these 
seizures  generally  appreciate  what  is  going  on  about  them,  and  will  often 
lespond  to  some  stern  order  for  them  to  cease  or  will  be  brought  to  a  state 
of  quietude  by  pressure  upon  some  part  of  the  body  which  provokes  pain. 
In  women  in  particular,  pressure  over  the  ovaries  or  epigastrium  will 
abort  the  attack;  the  application  of  cold  water  or  an  emetic  will  do  the 
same. 

After  a  hysterical  crisis  or  sudden  shock,  the  patient  may  be  found 
to  have  a  paralysis  of  arms  or  legs  or  one  side  of  the  body. 

The  Symptoms  of  the  Interparoxysmal  State.- — Between  the  crises 
of  major  hysteria  the  patient  may  be  in  a  fair  condition  of  general 
health,  but  usually  presents  certain  definite  chronic  manifestations  of 
the  disease. 

Sensory  Symptoms — These  consist  of  superiScial  and  deep  hyper- 
sesthesia  and  ansesthesia  and  anaesthetic  disturbances  of  the  special  senses. 
When  all  these  forms  of  anaesthesia  affect  one  side  of  the  body  we  have  a 
typical  major  hysterical  condition  which  may  last  for  years.  Cutaneous 
anaesthesia  occurs  in  three  forms:  the  common  form  is  that  of  hemian- 
aesthesia  involving  one-half  of  the  body;  next  in  frequency  is  the  segmental 
anaesthesia  involving  an  arm  or  a  leg  or  part  of  the  face  or  head;  rarest 
of  all  the  forms  is  a  disseminated  anaesthesia  occurring  in  the  form  of 
patches.  These  various  modes  of  distribution  are  shown  in  the  accom- 
panying figures.  The  anaesthesia  is  a  pain  anaesthesia  chiefly.  The 
tactile  and  thermic  sensations  are  less  markedly  affected.  Loss  of  deep 
sensibility  is  rare.  The  anaesthesia  is  in  some  cases  transferable  by 
means  of  magnets  or  electrical  irritants  or  by  suggestion.  The  anaes- 
thesia can  also  be  lessened  or  removed  temporarily  by  the  application 
of  magnets  or  coins  or  pieces  of  metal.  For  example,  if  a  silver  coin 
is  fastened  upon  the  anaesthetic  area,  in  the  course  of  a  few  minutes 


496 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


or  a  few  hours  there  will  be  a  zone  of  normal  sensation  under  and 
around  the  coin.  Sometimes  the  temperature  of  the  skin  upon  the 
ansesthesic  part  is  lowered  3°  or  4°  F.,  and  upon  pricking  the  skin  blood 
does  not  flow.  The  anaesthesia  is  oftener  upon  the  left  side  in  the  pro- 
portion of  three  to  one.  Hysterical  anaesthesias  are  not  accompanied 
by  subjective  sensations  as  are  organic  anaesthesias.  The  skin  reflex 
is  usually  abolished,  as  is  the  conjunctival  reflex.  The  deep  reflexes 
are  lessened  or  unchanged.  Anaesthesias  of  some  kind  occur  in  a  very 
large  proportion  of  the  serious  forms  of  hysteria  major.  They  are 
rare,  however,  in  children  and  are  rarer  in  women  than  in  men,  in  the 
author's  experience.  Anaesthesia  of  the  mucous  membranes  is  present 
chiefly  in  hemianaesthesia ;  it  then  involves  the  mucous  membrane  of 


Fig.  226. — Hysterical  loss  of  color  sense  and  limitation  of  visual  field.  Color  sense 
absent  in  left  eye  and  field  contracted;  in  right  eye  field  less  contracted;  order 
of  appreciation  of  colors  from  without  in  was  yellow,  violet,  blue,  red,  green. 


the  mouth  and  throat,  and  to  a  less  extent  that  of  the  nose  and  glottis. 
Hemianaesthesia  is  usually  accompanied  by  some  hemiplegia  and  often 
by  some  tremor.  Segmental  anaesthesia  is  also  often  accompanied  by 
some  degree  of  paralysis  of  the  part. 

Visual  anaesthesias.  One  of  the  most  common  of  the  permanent 
stigmata  of  hysteria  is  a  concentric  limitation  of  the  visual  field  and  a 
disturbance  in  the  color  sense.  Complete  loss  of  this  sense  may  take 
place  or  there  may  be  a  variation  in  the  ways  in  which  the  colors  are  per- 
ceived. There  may  be  also  a  distinct  diminution  in  the  acuity  of  vision 
or  even  a  complete  loss  of  sight  of  one  eye  or  both  eyes.  This  hysterical 
amblyopia  usually  comes  on  suddenly  and  may  last  for  weeks.  It  is 
not  always  a  true  blindness  and  the  patient  left  to  walk  about  a  room 
does  not  run  into  obstructions.     The  visual  disturbance  is  most  common 


THE    PSYCHO-NEUROSES 


497 


with  hemianaesthesia.  It  is  more  marked  on  the  affected  side,  but  exists 
to  some  extent  on  the  healthy  side.  The  Hmitation  of  the  fields  is  shown 
in  the  accompanying  cut  (Fig.  226). 

Hearing.  There  is  sometimes  a  diminution  in  the  acuity  of  hearing 
of  one  ear,  and  this  occurs,  if  present,  in  connection  with  hemianaesthesia. 
There  may  also  be  a  loss  of  hearing  to  high  and  low  notes,  while  hearing 
is  apparently  fairly  good  to  notes  of  medium  range;  and  finally  there  may 
be  a  diminution  in  hearing  by  bone  conduction,  while  hearing  by  aerial 
conduction  is  but  little  impaired,  this  being  due  probably  to  an  anaesthesia 
of  the  acoustic  nerve. 

Disturbances  of  taste  in  the  form  of  anaesthesia  or  paraesthesia  are 
quite  frequent  and  are  important  signs  in  hysteria.  The  loss  of  the  sense 
of  taste  may  involve  only  the  back  portion  of  the  tongue  and  the  palate. 

The  sense  of  smell  may  be  abolished,  but  this  usually  occurs  in  con- 
nection with  hemianaesthesia. 


Fig.  227. — The  three  types  of  distribution  of  anaesthesia  in  hysteria;  hemianaesthesia, 
segmental  and  disseminated.     Z,  hysterogenic  zones. 


Hyperaesthesias  and  neuralgias.  Pure  neuralgias  are  somewhat  rare 
in  true  hysteria,  but  hyperaesthesia  and  pains  of  various  kinds  are  not 
at  all  infrequent.  Hyperaesthesia  occurs  in  the  form  of  patches  at  differ- 
ent parts  of  the  body.  These  sensitive  points  may,  when  pressed  upon, 
bring  on  paroxysms  of  various  kinds,  and  they  are  therefore  called  the 
hysterogenic  zones  (Fig.  227).  The  most  common  seat  of  these  zones 
in  women  is  over  the  ovaries ;  in  men,  in  regions  corresponding  to  the  ova- 
ries and  on  the  scrotum.     Hysterogenic  zones,  however,  may  be  found 

32 


498  DISEASES    OF    THE    NERVOUS    SYSTEM 

just  beneath  the  mammary  gland,  on  the  epigastrimn,  along  the  spine, 
and  in  other  places.  These  zones  are  sensitive  areas;  they  can  be  made 
to  disappear  by  applications  of  electricity  and  by  refrigeration  and  coun- 
ter-irritation. Hysterical  patients  often  suffer  from  local  headaches, 
which  are  apt  to  be  confined  to  the  top  of  the  head  or  to  the  sides  near  the 
temples.  The  pain  is  severe,  sharp,  and  boring,  and  may  exacerbate 
with  such  intensity  as  to  produce  symptoms  almost  resembling  menin- 
gitis. The  spot-like  pains  are  known  as  hysterical  clavus.  There  may  be 
also  a  peculiar  persistent  local  pain  of  a  similar  nature  to  clavus  called 
topalgia  or  place-pain.  Hysterical  patients  occasionally  have  migraine, 
facial  neuralgia,  and  intercostal  neuralgia. 

Much  more  often  they  have  pains  along  the  spine,  producing  symp- 
toms of  spinal  irritation.  Hysterical  patients  also  have  at  times  attacks 
of  vagatonia  and  of  palpitation  and  pains  over  the  heart,  constituting 
what  is  known  as  pseudo-angina.  Such  troubles  are  much  more  frequent 
in  women. 

Arthralgias  are  painful  joints  in  which  the  condition  simulates  a 
chronic  arthritis  but  has  none  of  the  evidences  of  inflammation,  except 
sometimes  a  slight  oedema  or  effusion. 

Motor  Symptoms. — The  motor  symptoms  of  hysteria  are  paralyses, 
myasthenia,  contractures,  tremor,  and  choreic  and  ataxic  movements. 
The  paralyses  of  hysteria  take  the  form  of  hemiplegia,  paraplegia,  and 
monoplegias.  Hysterical  hemiplegia  occurs  usually  rather  suddenly, 
often  as  the  result  of  some  severe  shock.  The  left  side  is  more  frequently 
attacked.  The  arm  is  most  affected,  the  leg  next,  while  the  face  is  hardly 
ever  involved.  The  paralysis  is  not  an  absolute  one,  and  the  patient  is 
able  to  drag  himself  along.  The  deep  reflexes  are  usually  not  exaggerated 
and  they  may  be  for  a  short  time  absent.  The  paralysis  is  thus  a  flaccid 
one.  The  gait  of  the  patient  is  different  from  that  of  hemiplegia  due  to 
organic  disease;  in  hysterical  hemiplegia  the  patient  drags  the  paralyzed 
leg  after  him,  in  organic  hemiplegia  the  patient  swings  the  paralyzed  leg 
around  in  a  half-circle  (Fig.  228).  This  pecuharity  of  the  gait,  the 
absence  of  abnormal  reflexes,  the  absence  of  paralysis  of  the  face, 
and  the  presence  very  commonly  of  other  hysterical  stigmata  are 
sufficient  to  enable  one  to  make  the  diagnosis.  Sometimes  the  face  on 
the  affected  side  is  slightly  drawn  by  a  spasm,  so  that  it  appears  to  be 
paralyzed  when  it  really  is  not  (Charcot) .  Monoplegias  affect  the  arm 
or  leg,  very  rarely  indeed  the  face,  occasionally  the  eye  muscles,  and 
most  commonly  of  all  the  muscles  of  the  larynx.  Hysterical  monoplegia 
is  usually  accompanied  by  anaesthesia  of  the  affected  part  and  by  other 
symptoms  of  hysteria. 

In  children  hysterical  palsies  are  almost  always  monoplegic,  never 


THE    PSYCHO-NEUROSES 


499 


hemiplegic.  There  are  no  serious  atrophic  changes  or  disturbances  of 
the  electrical  reactions.  Hysterical  eye  palsies  show  themselves  in  the 
form  oftenest  of  an  insufficiency  of  the  internal  recti.  In  hysterical  palsy 
of  the  larynx  the  adductors  are  psychically  involved  so  that  the  patient 
cannot  speak  loud,  and  the  condition  is  called  hysterical  aphonia.  The 
trouble  often  comes  on  suddenly,  the  patient  finding  that  he  cannot  speak 
above  a  whisper.  The  paralysis  is  mental  and  therefore  the  adductors 
can  be  approximated  in  coughing.     The  trouble  is  distinguished  from 


Fig.  228  — -Hysterical  hemiplegia  showing  flaccidity  of  the  paralysis. — (Loiide.) 


laryngeal  inflammation  by  inspection  of  the  affected  part.  The 
tongue  and  other  muscles  of  articulation  are  in  very  rare  cases  also  in- 
volved, and  hysteria  may  produce  symptoms  resembling  a  bulbar  paral- 
ysis. Paraplegia  is  a  rather  uncommon  form  of  hysterical  palsy;  it  is 
usually  brought  on  by  emotions  of  depressing  character,  often  associated 
with  some  slight  injury.  It  may  be  accompanied  by  a  good  deal  of  pain 
in  the  back,  and  the  form  of  disease  which  was  once  known  as  "spinal 
concussion"  consisted  in  many  cases  of  hysterical  paraplegia  combined 
with  traumatic  disturbance  of  the  spine.     In  hysterical  paraplegia  there 


500 


DISEASES    OF    THE    NERVOUS    SYSTEM 


is  very  little  wasting  of  the  limbs  and  no  change  in  the  electrical  reac- 
tions. The  deep  reflexes  may  be  somewhat  increased  or  normal;  they 
are  never  absent.  There  is  never  any  prolonged  or  persistent  ankle  clonus, 
but  there  may  be  a  short  or  spurious  clonus  due  to  a  general  exaggerated 
irritability  of  the  nervous  system.  The  sphincters  are  never  involved 
except  temporarily  or  through  some  complication. 

Myasthenia  is  a  frequent,  peculiar,  and  interesting  symptom  occur- 
ring in  the  interparoxysmal  stage  of  hysteria.  It  consists  of  a  more  or 
less  temporary  feeling  of  weakness  of  an  arm  or  of  the  legs  or  whole  body. 


Fig.  229. — Hysterical  contracture  of  hand. 


Thus  a  person  in  lifting  a  dish  from  the  table  suddenly  feels  the  arm  give 
out,  and  if  not  careful  the  dish  is  dropped ;  or  while  walking  the  patients 
suddenly  feel  as  though  they  had  lost  all  power  in  the  lower  limbs.  This 
myasthenic  condition  is  generally  temporary,  but  it  may  be  so  permanent 
as  to  produce  a  certain  degree  of  monoplegia  or  paraplegia.  The  myas- 
thenic condition  may  precede  a  paralysis.  It  presents  no  objective  signs 
in  the  way  of  electrical  reaction;  it  involves  a  whole  member,  not  a 
single  group  of  muscles. 

Contractures.- — In  some  forms  of  hysteria  there  is  a  tendency  for  the 
muscles  to  undergo  contracture  under  slight  mechanical  stimulation, 
much  as  pressure  or  a  blow.  This  tendency  to  contracture  in  hysteria 
is  called  the  contractural  diathesis,  and  it  is  an  important  sign.  The 
contractures  may  be  temporary,  disappearing  soon  after  the  exciting 
cause  ceases,  or  they  may  develop  independently  and  last  for  a  long 
time.  They  usually  but  not  always  disappear  in  sleep,  and  under 
anaesthesia.     They  involve  the  legs,  arms,  and  facial  muscles,  and  may 


THE    PSYCHO- NEUROSES  501 

be  associated  with  paralysis  and  anaesthesia  (Figs.  229,  230).     The  con- 
tracture is  usually  a  spasmodic,  not  a  paralytic  one. 

Tremor  occurs  in  hysteria  in  a  considerable  proportion  of  cases, 
more  especially  those  in  which  there  are  hemiplegia  and  hemiansesthesia. 
Hysterical   tremor  simulates  all  the  various  types.     The  common  form 


Fig.  230. — Hysterical  contracture  of  toe. 

is  one  in  which  the  oscillations  occur  from  five  and  a  half  to  seven  and 
a  half  times  a  second,  and  is  jerky  and  irregular  in  type.  It  ceases 
for  a  time  when  the  person  is  quiet  or  lies  in  the  horizontal  position; 
also  during  sleep.  It  affects  the  head  and  tongue  as  well  as  the  ex- 
tremities, the  latter  more  upon  one  side  than  the  other.  It  may  be  chiefly 
in  the  lower  limbs.  Sometimes  it  has  the  type  of  an  intentional  tremor, 
ceasing  on  rest  of  the  hand  and  increasing  when  the  hand  is  moved,  as 


Repose.  Movement. 

Fig.  231. — Illustrating    intentional    tremor   in    hysteria.     (Tourette.) 

in  raising  a  glass  to  the  lips  (Fig.  231).  It  then  resembles  exactly  the 
tremor  of  multiple  sclerosis.  There  may  be  a  slow  tremor  of  four  to  five 
and  a  half  oscillations  per  second;  this  persists  during  rest  and  is  but 
little  modified  by  voluntary  movements.  It  imitates  the  tremor  of 
paralysis  agitans.  Finally,  there  may  be  a  rapid  tremor  of  eight  to  nine 
oscillations  per  second.  This  also  persists  during  repose  and  is  but  little 
modified  by  movements.  It  imitates  the  tremor  of  Basedow's  disease, 
alcoholism,  and  neurasthenia. 


502  DISEASES    OF    THE    NEEVOUS    SYSTEM 

Trophic  Disorders. — -In  hysterical  paralysis  a  slight  amount  of  atrophy 
occurs,  but  only  such  as  would  naturally  follow  disuse  of  the  part. 
Cutaneous  eruptions  and  dystrophies  practically  do  not  exist  or,  if  pres- 
ent, are  the  result  of  complicating  disorders. 

Visceral  Symptoms. — Hysterical  patients  often  suffer  from  dyspepsia 
and  constipation,  also  from  anorexia,  and  in  some  cases  from  vomiting 
or  regurgitation  of  food.  Occasionally  the  anorexia  and  vomiting  be- 
come persistent;  the  patient  refuses  food  or  rejects  all  that  is  taken;  she 
emaciates,  becomes  weak  and  bedridden,  and  develops  into  that  partic- 
ular phase  of  hysteria  known  as  anorexia  nervosa.  In  these  cases,  along 
with  the  aversion  to  food  and  vomiting,  there  may  be  a  great  deal  of 
gastralgia. 

The  urine  in  hysteria  is  apt  to  be  of  low  specific  gravity.  Some- 
times there  is  retention  of  urine;  in  extremely  rare  cases  there  is  a  con- 
dition known  as  ischuria  and  anuria,  in  which  for  several  days  extremely 
small  quantities  of  urine  are  passed,  owing  apparently  to  a  suspension 
of  the  functions  of  the  kidney.  Such  cases  should  always  be  carefully 
investigated. 

Vasomotor  symptoms  are  very  common.  The  autonomic  and  sympa- 
thetic tonus  is  often  involved,  causing  vaso-vagal  attacks  and  gastro- 
intestinal disturbance  with  pain,  diarrhoea  and  vomiting.  These  dis- 
turbances of  the  sympathetic  are  also  shown  by  flushings  and  pallor, 
cold  extremities,  and  at  times  an  oedematous  condition  of  one  or  more 
extremities.  This  oedema  may  be  of  the  ordinary  pale,  waxy  character, 
pitting  upon  pressure.  In  other  cases  it  has  a  peculiar  bluish  tinge  and 
it  does  not  pit;  the  hands,  which  are  the  parts  generally  affected,  are 
several  degrees  below  the  normal  in  temperature,  and  the  limb  resembles 
in  some  respects  the  condition  in  Raynaud's  disease.  Gangrene,  how- 
ever, never  supervenes.  This  form  of  oedema  is  known  as  the  blue 
oedema  of  hysteria. 

There  occur  in  hysteria  febrile  attacks,  and  much  has  been  written 
upon  the  subject  of  hysterical  fever,  which  does  not  exist. 

Hystero-epilepsy. — ^The  form  of  hysteria  which  shows  itself  by  the 
development  of  severe  crises  known  as  hystero-epileptic  attacks  is 
extremely  rare  in  this  country,  at  least  in  its  typical  phase.  It  has 
been  particularly  studied  by  the  French  writers  Charcot,  Richer,  and 
others.  Hystero-epilepsy,  as  this  form  of  the  disease  is  called,  is  a 
true  hysteria  and  not  epilepsy  at  all,  nor  a  mixture  of  hysteria  and 
epilepsy,  though  the  name  would  suggest  that  that  was  the  case.  The 
typical  attacks  of  hystero-epilepsy  begin  with  certain  prodromata 
consisting  of  a  feeling  of  malaise  and  irritability  which  may  last  for 
several  hours  or  a  day. 

There  is  next  the  epileptoid  phase,  lasting  from  one  to  three  minutes; 


THE    PSYCHO-NEUROSES  503 

third,  a  phase  of  contortions  and  grand  movements,  lasting  one  to  three 
minutes;  fom^th,  an  emotional  phase,  lasting  from  five  to  fifteen  minutes; 
and,  finally,  a  stage  of  delirium,  lasting  a  variable  time;  the  whole 
attack  lasting  from  five  to  twenty  minutes.  In  this  country  we 
occasionally  see  hysterical  patients  exhibiting  one  or  two  of  these 
phases,  but  very  rarely  indeed  do  they  ever  go  through  the  whole  series. 
The  patients  who  suffer  from  hystero-epileptic  attacks  generally  during 
the  interparoxysmal  stage  present  many  of  the  stigmata  of  hysteria, 
such  as  paralyses,  contractures,  and  anaesthesias. 

Hysterical  crises  which  take  the  form  of  convulsions  or  emotional 
seizures  sometimes  end  or  are  associated  with  attacks  of  catalepsy  or 
trance  or  attacks  of  amnesia  and  cerebral  automatism.  As  these  con- 
ditions all  occur  in  other  diseases  than  hysteria,  they  will  be  described 
elsewhere  in  connection  with  the  subject  of  the  disorders  of  sleep  and 
of  consciousness. 

Hysterical  persons  occasionally  are  attacked  with  violent  and  per- 
sistent hiccoughing  or  sneezing.  Sometimes  also  there  come  on  attacks 
of  extremely  rapid  breathing  or  hysterical  polypnoea,  during  which 
the  respirations  run  up  to  fifty  or  seventy  a  minute.  A  hysterical  cough 
sometimes  occurs;  and  lasts  for  a  long  time.  (Esophageal  spasm  with 
consequent  dysphagia  is  another  one  of  the  somewhat  rare  phenomena 
of  hysteria.  Indeed,  many  of  the  symptoms  referred  to  in  this  last  para- 
graph may  be  grouped  as  tics  or  morbid  mental  habits,  and  not  truly 
hysterical. 

Pathology. — There  is  no  known  anatomical  change  at  the  basis  of 
hysteria.  We  do  not  find  the  marks  of  degeneration  as  we  do  in  serious 
forms  of  insanity  and  epilepsy. 

Diagnosis. — The  essential  characteristics  are  the  peculiar  emo- 
tional condition  of  the  patient,  the  past  history  of  hysterical  crises,  the 
presence  of  the  stigmata  of  hysteria,  such  as  anaesthesias,  limitation  of 
the  visual  field,  paralyses,  and  contractures.  The  variability  of  the 
symptoms,  their  susceptibility  to  influence  under  suggestion  and  rigorous 
moral  measures,  the  absence  of  organic  disease  or  of  serious  disturbance 
of  nutrition,  the  sex  and  age,  and  the  cause  should  also  have  weight  in 
guiding  us  to  our  decision. 

The  test  of  hysteria  minor  is  simply  the  presence  of  a  morbidly  easy 
reaction  of  the  mind  upon  the  body.  It  has  no  absolute  criteria.  What 
is  morbid  must  be  determined  by  the  judgment  of  the  physician  con- 
sidering the  education  and  environment.  Hysteria  major  is  a  rare 
disease  and  has  a  clear-cut  syinptomatology.  It  has  crises  and  the 
stigmata  already  described. 

Hysteria  and  Paychasthenia.- — -If  a  person  has  an  obsession  or  fixed 
idea  which  consciously  affects  his  mind  and  actions,  but  not  directly  his 


504  DISEASES    OF   THE    NERVOUS    SYSTEM 

body  or  functions,  he  has  psychasthenia,  or  an  obsessive  psychoneurosis. 
The  obsession  in  hysteria  is  usually  a  subconscious  one;  in  psychasthenia 
it  is  conscious. 

Diagnosis  of  special  sympto7ns  of  hysterical  manifestations.  Hys- 
terical paralysis  is  characterized  by  the  fact  that  there  is  no  marked 
degree  of  wasting  of  the  muscles,  no  electrical  reactions  of  degeneration, 
the  deep  reflexes  are  preserved  or  exaggerated,  and  other  marks  of  hysteria 
are  present.  Hysterical  anaesthesia  can  generally  be  lessened  over  certain 
areas  by  the  application  of  the  magnet  or  can  be  made  temporarily  to 
disappear;  it  is  peculiarly  distributed  in  the  way  described  under  symp- 
toms and  is  associated  with  anaesthesias  of  the  special  senses.  Hysterical 
contractures  sometimes  cease  during  sleep  and  generally  under  deep  nar- 
cosis, and  the  use  of  an  anaesthetic  may  clear  up  the  case.  They 
usually  follow  a  fit,  an  injury,  or  an  operation.  They  are  somewhat 
increased  on  attempts  to  overcome  them  by  force;  they  are  usually 
associated  with  paralysis  and  anaesthesia  and  other  hysterical  symptoms. 

Hysterical  convulsions.  These  differ  from  convulsions  of  epilepsy 
in  the  way  best  indicated  by  the  following  table : 

Hysterical  Convulsions  Epileptic  Convulsions 

Brought  on  by  the  emotion  or  injury;  The  opposite  in  all  these  particulars, 
rarely  any  aura;  no  initial  cry;  move- 
ments co-ordinate;  tongue  not  bitten, 
and  patient  never  injures  herself. 
Duration  perhaps  several  hours  with 
intermissions;  consciousness  generally 
preserved.  Micturition  and  defeca- 
tion do  not  occur.  No  rise  of  tempera- 
ture; may  be  stopped  artificially. 
Rarely  occur  in  sleep. 

Although  the  differentiation  here  made  usually  holds  good,  there  occur 
psychogenic  convulsions  in  which  all  the  phenomena  of  the  epileptic 
fit  are  present. 

The  hystero-epileptic  attacks  are  so  characteristic  that  a  mistake 
could  not  be  made. 

Prognosis. — The  prognosis  of  hysteria  in  children  is  good.  They 
generally  get  well,  though  in  some  cases  there  is  a  recurrence  later  in 
life.  Minor  hysteria  under  proper  treatment  usually  gets  well  or  at 
least  is  of  little  importance.  The  major  forms  when  chronic  are  often 
intractable  even  under  the  best  treatment.  When  a  severe  form  of 
hysteria  occurs  in  a  person  of  feeble  frame  who  is  surrounded  with  a 
sympathetic  family,  the  task  of  rescuing  her  from  her  disorder  is  a  very 
arduous  one.  Traumatic  forms  of  hysteria  which  are  not  infrequently 
associated  with  some  actual  physical  injury  are  sometimes  difficult  to 
cure.     Hysteria  which  is  associated  with  some  organic  disease,  such  as 


THE    PSYCHO-NEUROSES  505 

a  severe  pelvic  disorder  or  an  organic  affection  of  the  central  nervous 
system,  has  a  poor  prognosis.  Hysteria  in  the  male  is  generally  curable, 
but  it  requires  vigorous  treatment,  and  spontaneous  cure  is  by  no  means 
likely  to  happen.  Major  hysteria  has  a  vastly  better  prognosis 
if  proper  treatment  for  it  is  instituted  early. 

Treatment. — The  treatment  of  hysteria  maybe  divided  into  mental, 
mechanical  dietetic,  and  medicinal  measures. 

By  all  odds,  the  most  important  factor  in  the  treatment  of  hysteria 
is  the  mental  treatment,  and  the  most  important  primary  measure  to  be 
taken  is  the  isolation  of  the  patient.  She  should  be  placed  where  she  will 
not  be  surrounded  by  sympathetic  friends;  where  life  will  be  a  regular 
one;  where  some  occupation  may  be  given  which  will  engross  attention, 
interest  the  mind,  and  call  into  play  the  physical  activities. 

In  the  major  forms  of  hysteria  associated  with  anorexia,  emaciation, 
anaemia,  and  possibly  pelvic  disorders,  the  "rest  cure"  as  elaborated  and 
carried  out  by  Weir  Mitchell  forms  by  all  odds  the  most  successful 
means  of  treatment.  In  many  cases  of  less  severe  character  a  partial 
rest  cure  in  which  the  patient  is  separated  from  her  family  but  is  not 
placed  under  such  severe  restrictions  may  be  all  that  is  needed.  In  the 
case  of  children  removal  from  home  is  often  advisable,  and  the  discipline 
of  well-conducted  schools  is  a  most  excellent  measure.  Re-educational 
treatment  by  therapeutic  talks,  by  direct  and  indirect  suggestion,  by 
occupation,  work,  marriage,  learning  a  craft  or  business;  life  in  a  sane 
environment,  these  are  the  real  methods  of  cure.  Psychoanalysis  and 
the  method  of  Freud  have  their  adherents. 

The  mechanical  means  used  in  hysteria  are  hydrotherapy,  electricity, 
massage,  and  exercise,  and  they  have  symptomatic  value.  Of  these 
measures  hydrotherapy  and  electricity  take  the  first  rank.  In  hydro- 
therapy the  douche  or  jet  to  the  back,  the  shower  and  cold  plunge, 
and  the  half-bath  are  the  most  efficacious.  In  the  electrical  treatment 
the  static  and  faradic  currents  give  some  results.  The  static  sparks  often 
relieve  contractures  and  lessen  or  remove  the  anaesthesias,  and  both 
forms  of  electricity  seem  to  have  a  generally  beneficial  tonic  effect. 
Doubtless  the  psychic  element  is  the  most  important  factor  in  this 
as  in  other  mechanical  measures.  Massage  is  of  some  value  in  pro- 
moting nutrition  and  it  also  has  a  favorable  sedative  effect  on  many 
cases.  Exercise,  particularly  of  an  active  kind,  such  as  stimulates  the 
mind  and  interests  one,  is  a  measure  of  extreme  value  and  one  which 
has  perhaps  not  been  sufficiently  appreciated. 

The  drugs  which  can  be  recommended  in  hysteria  are  not  numerous 
and  their  power  is  limited.  Valerianate  of  zinc,  asafoetida,  iron,  and  the 
bromides  are  the  most  important  of  the  nervines.  In  hysterical  children 
a  capsule  containing  two  grains  of  valerianate  of  zinc  and  one  of  sulphate 


506  DISEASES    OF    THE    NEEVOUS    SYSTEM 

of  quinine  is  often  efficacious.  Gowers  places  more  reliance  upon  the 
oil  of  turpentine  in  doses  which  should  be  increased  to  the  point  of 
strangury. 

In  the  treatment  of  hysterical  convulsions  the  most  efficient  measure 
is  the  administration  of  an  emetic,  and  this  can  be  best  done  by  giving 
hypodermically  one-twelfth  or  more  of  a  grain  of  apomorphine.  Con- 
vulsions can  be  stopped  sometimes  by  throwing  water  in  the  face  or  on 
the  epigastrium;  by  firm  and  somewhat  long-continued  pressure  over  the 
ovaries;  by  the  administration  of  valerian,  aromatic  spirits  of  ammonia, 
or  compound  spirits  of  ether. 


CHAPTER  XXII 
PSYCHASTHENIA 

Psychasthenia  is  a  chronic,  non-dementing  psychosis,  characterized 
by  the  occurrence  of  imperative  ideas  by  compulsive  and  impulsive  acts, 
by  morbid  fears  and  conditions  of  agitating  doubt.  The  term  obsessive 
neurasthenia  or  obsessive  psycho-neurosis  is  used  by  some  instead  of 
psychasthenia.  Beard  originally  described  many  of  these  symptoms  and 
classed  them  under  the  head  of  neurasthenia.  Indeed,  neurasthenia 
usually  accompanies  the  condition,  and  many  unstable  people,  when  they 
get  weakened  or  exhausted  by  work  or  disease,  develop  morbid  fears  and 
obsessions.  So  that  part  of  the  cure  of  psychasthenia  is  to  treat  the 
neurasthenia. 

Etiology. — The  most  frequent  etiological  factor  is  heredity;  nearly 
one-half  of  my  cases  gave  a  history  of  direct  or  indirect  mental  disorder 
in  the  ancestry.  I  have  seen  several  cases  in  which  the  obsessive 
psychosis  occurred  in  mother  and  son  or  mother  and  daughter. 

Lues,  tuberculosis,  and  alcoholism  occur  in  the  ancestry,  but  not  so 
prominently  as  in  other  psychoses.  The  disease  occurs  in  males  and  fe- 
males about  equally.  Symptoms  of  the  trouble  may  be  shown  in  children 
as  young  as  eight  or  nine  years;  more  than  half  the  cases,  however,  de- 
velop between  the  ages  of  fifteen  and  twenty-five;  nearly  one-fourth  of 
the  cases  between  the  ages  of  twenty-five  and  thirty,  while  one-eighth 
of  the  cases  develop  between  the  ages  of  ten  and  fifteen.  A  few  cases 
occurred  between  the  ages  of  thirty-five  and  forty,  and  it  is  seen  again 
with  some  frequency  at  the  time  of  the  climacteric.  I  have  seen  three 
cases  in  which  the  disease  developed  after  the  age  of  sixty.  The  earlier  the 
case  develops,  the  more  persistent,  as  a  rule,  are  the  symptoms  liable  to 
become. 

Among  the  most  frequent  exciting  causes  may  be  mentioned  some 
kind  of  shock  by  fall  or  accident;  next  after  this  is  alcoholic  excess. 
Among  other  causes  I  have  noted  infectious  fevers,  an  attack  of  chorea, 
a  stroke  of  lightning,  car  sickness,  educational  strain.  Engagements, 
marriage  and  pregnancy  have  been  rather  often  a  starting  point  of  the 
disease. 

Symptoms. — The  symptoms  develop  in  four  different  types,  though 
these  are  often  intermingled,  and,  in  most  cases  at  least,  three  of  the 

507 


508  DISEASES    OF    THE    NERVOUS    SYSTEM 

characteristic  groups  of  symptoms  are  more  or  less  present.^  These 
types  are  those  characterized  by  (1)  morbid  fears,  (2)  by  imperative 
ideas,  (3)  by  a  doubting  mania,  and  (4)  by  morbid  impulses. 

In  91  cases  I  find  the  order  about  as  follows:  Morbid  fears,  37; 
obsessive  and  fixed  ideas,  25;  doubting  manias,  18;  compulsions  and 
impulsions,  11.  Psycho-analysis  may  show  that  these  different  groups 
have  a  different  mechanism,  but  my  experience  is  that  they  are  clinically 
often  allied  and  intermingled. 

Morbid  Fear,  Doubting  Mania. — This  disorder  begins  usually  rather 
suddenly  as  a  result  of  some  slight  shock,  and  perhaps  of  some  causal 
and  unimportant  incident.  A  young  man,  while  in  church,  or  in  a  crowd, 
suddenly  has  a  feeling  of  disturbance  of  consciousness,  with  something 
akin  to  vertigo.  He  is  alarmed,  the  head  seems  full,  the  heart  palpitates, 
and  he  feels  as  if  he  would  faint.  These  attacks  may  be  repeated.  They 
have  been  called  psychic  seizures,  or  psycholepsy.  Some  of  these  seizures 
appear  to  be  psychogenous  vago-tonic  attacks.  After  one  occurs  the 
patient  becomes  afraid  to  go  in  a  crowd  (agoraphobia)  or  in  an  enclosed 
place  where  there  are  people  (claustrophobia;  he  may  even  be  afraid  to  go 
out  of  doors  without  a  companion.  This  state  is  accompanied  with 
some  general  nervousness,  depression,  insomnia,  and  pressure  or  pain  at 
the  back  of  the  head  or  vertex.  He  is  often  unable  to  pursue  his  work 
or  study,  and  becomes  worrying  and  introspective.  After  some  months 
or  a  year  the  secondary  symptoms  disappear,  but  he  may  for  several 
years  feel  a  dread  of  going  in  certain  places. 

Fear  of  storms  and  of  lightning  (astraphobia)  may  come  on  in  much 
the  same  way,  but  this  form  of  morbid  fear  is  less  disturbing  as  a  rule, 
and  often  the  patients  are  quite  well  as  long  as  the  sky  is  reasonably 
clear.  Some  patients  are  so  sensitive,  however,  that  they  become 
nervous  and  depressed  before  storms,  and  can  predict  them  as  unerringly 
as  do  rheumatic  or  neuralgic  sufferers. 

In  fear  of  contamination  and  dirt  (mysophobia)  the  patient  is  con- 
stantly washing  the  hands,  changing  the  clothes,  and  trying  to  avoid 
contact  with  people.  The  sufferer  will  spend  an  hour  or  more  in  dressing 
and  undressing  or  in  preparing  to  go  out.  After  a  time  almost  all 
activity  is  curtailed  by  dread  of  contact  with  something,  and  the  victim 
sits  in  a  chair,  or  lies  in  bed  with  hands  enveloped  in  cloths  to  protect 
him  from  the  dust.  All  the  interests  of  life  are  lost  in  this  one  absorb- 
ing idea  and  fear,  though  the  patient  is  not  demented  or  maniacal. 

^  The  condition  of  obsessive  and  fixed  ideas  has  been  called  compulsive  in- 
sanity. Compulsive  acts  may  result,  but  they  are  accompanied  by  consciousness  of 
the  nature  of  the  act,  by  feelings  of  anxiety,  and  by  attempts  at  resistance.  The 
victim  of  morbid  impulses  is  said  to  be  suffering  from  impulsive  insaniiy.  Here  the 
impulses  spring  suddenly  into  consciousness,  and  acts  follow  at  once  without  the 
patient  being  able  to  resist  them.  These  impulses  vary  in  character  and  severity 
from  the  impulse  to  touch  a  lamp  post  to  that  to  commit  a  murder. 


PSYCHASTHENIA  509 

There  is  a  decided  depression,  but  not  a  true  melancholia.  If  the  patient, 
however,  is  driven  by  .his  attendants  to  do  things  he  dreads,  he  cries  and 
becomes  excited  and  hysterical. 

Fear  that  the  heart  may  stop  or  the  breathing  cease  are  also  serious 
types  of  morbid  fear.  The  patient  is  always  feeling  the  pulse  and  asking 
for  an  examination  of  the  heart  and  an  assurance  of  its  soundness. 

The  number  of  fears  is  almost  as  great  as  the  number  of  objective 
things.  The  more  common  types  are  mysophobia,  agoraphobia,  claus- 
trophobia, fear  of  riding  in  cars  or  carriages  (in  New  York  City  of  sub- 
ways) and  astraphobia.  There  are  also  many  ''occupation  fears,"  such 
as  that  in  which  the  barber  fears  to  use  his  razor,  the  tailor  to  cut  the 
cloth,  the  bartender  to  mix  drinks,  and  the  business  man  to  sign  his  name 
to  checks.  These  symptoms  lun  a  course  of  one-half  to  three  years.  If 
properly  treated,  the  patient  recovers,  with  a  tendency  to  relapse. 

Allied  to  the  morbid  fears  are  the  morbid  "philias"  or  anxious 
concern  for  the  safety  and  health  of  the  race,  more  particularly  of  the 
domestic  animals.  The  patients  cannot  walk  the  streets  without  con- 
cern over  the  tail  of  the  docked  horse  and  will  get  up  at  night  to  fetch 
in  a  wailing  cat  which  seems  to  him  in  real,  not  amorous,  distress 
(zoophilia) . 

While  morbid  fears  occur  in  very  early  life,  often  developing  at 
puberty,  doubting  mania  occurs  rather  later,  usually  after  adolescence. 
The  doubting  habit  is  often  a  morbid  outgrowth  of  an  original  morbid 
scrupulosity  and  attention  to  detail.  The  patient  has  usually  been  very 
orderly  in  habit  and  worried  when  things  are  not  arranged  or  done  in  a 
very  orderly  way.  The  clothes  and  bureau  drawers  and  the  bric-a-brac 
of  the  room  have  all  their  set  place,  and  a  discomfort  is  felt  at  seeing 
them  out  of  the  regular  spot.  Then  some  disturbing  emotion  or  sickness 
sets  agoing  an  absolute  distress  of  mind  if  things  are  not  just  so  or  are 
not  perfectly  clean.  Then  begin  frequent  washings,  change  of  clothes, 
an  hour  is  spent  in  arranging  the  articles  on  a  bureau  and  mantle  or  in 
dressing  the  hair. 

The  doubting  mania  sometimes  seizes  girls — -more  rarely  men — ■ 
who  are  about  to  be  married,  and  engagements  are  repeatedly  made 
and  broken.  Often  the  doubting  habit  is  shown  in  connection  with 
fear  of  fire,  of  burglars,  or  gas.  The  patient  gets  up  at  night  a  dozen 
times  to  feel  the  gas  jets,  to  see  if  the  doors  are  locked,  to  look  under 
the  bed,  and  do  other  whimsical  things.  These  doubting  states  are 
often  not  very  serious,  and  are  only  exaggerations  of  a  naturally  timid 
and  scrupulous  disposition.  Alcoholism  is  at  times  associated  with 
doubting  mania. 

Obsession,  Fixed  Idea. — Obsessions  and  fixed  ideas  often  relate  to 
some  rather  trivial  thing.     In  the  obsessive  constitution  the  association 


510  DISEASES    OF   THE    NERVOUS    SYSTEM 

machinery  seems  to  get  clogged  and  ideas  tend  to  stick  pertinaciously  in 
the  mind.  A  slight  suggestion  or  remark  casually  made  with  some 
especial  rhythm  or  emphasis  stays  and  bothers  the  patient.  More 
often  there  are  one  or  more  ideas  which  stay  and  torment  him.  They 
are  unpleasant  ideas  of  possible  mistakes  made  or  injuries  thought  to 
have  been  done.  They  are  usually  absurd,  and  the  patient  knows  per- 
fectly well  that  they  are  so,  but  they  cannot  be  shaken  off.  They  domi- 
nate and  harass  the  sufferer  who  feels  really  like  one  "  possessed."  They 
lead  to  insomnia,  nervous  restlessness,  hysterical  outbreaks,  and  crises  of 
the  abdominal  viscera,  with  diarrhoea  and  polyuria.  Yet  often  the 
patient,  if  naturally  intelligent  and  sensible,  will  keep  himself  in  control, 
and  show  most  of  the  time  no  emotion  or  evidence  of  suffering.  These 
fixed  ideas  may  attack  a  person  periodically  for  years,  or  may  after  a 
few  months  disappear,  not  recurring  at  least  to  any  extent.  Shocks, 
acute  sickness,  and  depressing  experiences  will  bring  them  out. 

The  syndrome  of  the  fixed  idea,  not  reaching  the  intensity  of  a  delu- 
sion, may  be  part  of  a  melancholia  of  involution  or  of  manic-depressive 
insanity. 

Morbid  Impulse. — Impulsive  psycho-neurosis  is  the  condition  in 
which  impulses  spring  suddenly  into  consciousness,  and  acts  follow  at 
once  without  the  patient  being  able  to  resist  them.  The  morbid  im- 
pulses may  be  very  slight  and  harmless,  such  as  a  desire  to  touch  every 
lamppost  passed  on  the  street,  to  step  on  alernate  stones  of  the  pavement, 
to  put  the  left  foot  first  in  going  from  a  room,  or  they  may  lead  to  violent 
acts,  such  as  murder,  theft,  or  arson.  When  there  is  a  morbid  impulse 
to  utter  certain  words  over  and  over,  it  is  called  onomatomania.  Psychic 
tics  belong  to  the  morbid  impulses.  A  patient  of  mine,  a  clergyman, 
who  was  overworked  and  anxious,  developed  impulses  to  an  automatic 
coprolalia  and  profanity  while  at  work  in  his  study,  and  even  while 
preaching.  Another  clergyman  had  the  same  tendency  along  with  a 
decided  doubting  mania. 

Morbid  Compulsion. — When  a  morbid  impulse  rises  into  conscious- 
ness and  is  held  more  or  less  under  restraint  it  is  called  rather  artificially 
a  compulsion.  A  patient  while  shaving  started  to  cut  himself.  He 
never  did  do  this,  though  he  was  obliged  to  give  up  doing  this  function 
himself  for  a  time.  He  also  felt  an  intense  desire  to  jump  overboard 
while  on  a  ship,  though  he  had  had  no  melancholia  at  any  time.  The 
compulsion  is  often  perfectly  restrained,  and  I  have  known  a  man  who 
went  about  for  years  with  at  times  an  almost  overwhelming  fear  that  there 
would  come  upon  him  an  uncontrollable  impulse  to  assault  some  one. 

Compulsive  and  Impulsive  Manias. — When  impulses  and  compulses 
involve  a  larger  psychical  sphere,  we  have  the  various  conditions  known 
as  kleptomania  and  pyromania,   homicidal  and  suicidal  mania.     But 


PSYCHASTHENIA  511 

here,  along  with  defective  inhibition,  there  is  often  a  morbid  degree  of 
criminal  instinct  or  there  may  be  present  another  psychosis,  such  as 
mania  or  melancholia  or  paranoia.  Thus  the  sexual  criminal  acts  and 
perversions  are  of  the  class  of  compulsions  or  impulsions,  plus  a  con- 
genital and  hereditary  instinctive  defect. 

A  type  of  impulsion  midway  between  the  mild  and  neurasthenic 
and  the  deep-seated  psychopathic  cases  are  the  impulses  to  drink  leading 
to  periodical  inebriety.  Here  there  occurs  periodically,  with  or  without 
the  excitement  of  a  single  taste  of  liquor,  an  overwhelming  impulse  to 
drink,  and  the  patient  drinks  until  consciousness  is  lost. 

In  fine,  impulsive  and  compulsive  insanity  are  generally  part  of 
the  psycho-neurosis  but  they  may  occur  as  episodes  in  melancholia, 
mania,  dementia  prsecox,  paranoia,  and  the  criminal  constitution. 

Hypochondriasis  and  Psychasthenia. — Hypochondriasis  is  a  term 
applied  to  a  morbid  mental  condition  in  which  the  patient  thinks  he 
is  suffering  from  some  physical  disease.  It  is  a  much  used  and  much 
abused  term.  Hypochondriacs  vary  much  in  the  degree  in  which  the 
symptoms,  show  themselves.  In  some  cases  the  belief  in  the  disease  is 
so  foolish  and  extravagant  as  to  form  a  real  delusion,  as  when  a  patient 
thinks  he  has  a  worm  in  the  head  or  stomach  or  an  absolute  and  permanent 
stoppage  of  the  bowels.  In  these  cases  the  hypochondria  is  only  a 
manifestation  of  a  melancholia,  generally  a  chronic  melancholia  of 
involution. 

In  more  cases  the  patient's  hypochondria  is  simply  a  manifestation 
of  a  morbid  fear  or  an  idee  fixe  or  obsession.  These  are  cases  of  psychas- 
thenia. A  mild  degree  of  hypochondria  often  characterizes  chronic 
neurasthenia.  Hypochondriasis,  therefore,  is  only  a  syndrome  which 
occurs  in  melancholia,  psychasthenia  and  neurasthenia,  and  is  not  a 
separate  disease. 

Hysteria  and  Psychasthenia. — Some  at  least  of  the  mental  traits  and 
emotional  crises  of  hysteria  are  forms  of  or  episodes  of  psychasthenia. 
There  is  here  a  loss  of  control  due  to  the  sudden  explosion  of  fear  or  anger 
from  an  inadequate  cause.  The  interparoxysmal  state  of  the  hysterical 
is  characterized  often  by  morbid  fears  and  obsessions  and  by  psychic  tics. 
Thus  the  psychasthenic,  who  despite  his  morbid  fears  is  forced  to  do  things 
he  dreads,  will  go  into  an  emotional  crisis  resembling  an  hysterical 
attack. 

Diagnosis. — The  diagnosis  of  a  psychasthenia,  characterized  by 
morbid  doubts  and  fears,  fixed  ideas  and  morbid  impulses,  is  usually 
very  easy.  Sometimes  the  condition  is  associated  with  a  great  deal  of 
mental  depression  and  anxiety,  so  that  it  may  be  something  like  a 
melancholia;  but  there  is  with  it  none  of  the  profound  melancholia,  with 
suicidal  feelings,  and  the  condition  is  one  more  of  anxiety  and  alarm  than 


512  DISEASES    OF    THE    NERVOUS    SYSTEM 

of  true  emotional  depression.  There  is,  furthermore,  no  difficulty  or 
retardation  of  thought,  nor  any  of  the  apathy  of  melancholia.  Persons 
with  fixed  ideas  or  obsessions  may  seem  at  first  to  resemble,  to  a  certain 
extent,  paranoiacs,  and  such  cases  have  been  described  as  abortive  types 
of  paranoia.  The  fixed  idea,  however,  is  one  which  the  patient  realizes 
to  be  over-dominant  and  in  a  sense  forced  upon  him;  he  does  not  accept  it 
with  sympathy  and  conviction  as  the  paranoiac  does;  he  is  aware  that  it 
is,  in  a  measure,  delusional  in  character.  In  the  case  of  morbid  impulsive 
acts,  the  question  of  an  underlying  melancholia  or  other  psychosis  must 
be  considered.  The  splitting  up  of  the  various  clinical  symptoms  into 
special  groups  of  anxiety  psychosis,  conversion  hysteria,  true  (actual) 
neuroses,  psycho-neuroses  is  a  matter  for  psychologists.  It  does  not  seem 
to  me  necessary. 

Prognosis. — ^Psychasthenia  associated  with  morbid  fears  and  doubt- 
ing manias,  occurring  in  early  life,  is  a  serious  condition.  If  taken  early 
in  Jiand,  however,  and  placed  under  rigid  control,  the  patients  have  an 
excellent  chance  of  recovering  in  one  or  two  years.  If,  as  is  often  the 
case,  the  patients  are  kept  at  home  and  not  properly  managed,  the  trouble 
becomes  fixed,  some  mental  deterioration  develops,  and  a  serious  and 
incurable  condition  takes  place. 

When  the  disease  develops  later  in  life,  as  an  episode  or  as  the  result 
of  some  shock  or  exhausting  effort,  prompt  treatment  is  usually  effective; 
but  here  again,  if  the  trouble  be  neglected  and  becomes  fixed,  the  prognosis 
is  more  serious. 

Psychasthenic  conditions  associated  with  fixed  ideas  and  compulsions 
are  in  my  experience  less  serious.  They  often  disappear  under  tonic 
treatment  and  rest  in  the  course  of  a  few  months  or  a  year,  but  there  is 
the  liability  that  they  may  return. 

An  obsessive  psychosis  rarely  develops  in  the  degenerative  period  of 
life;  if  it  does,  it  is  serious  and  is  apt  to  turn  out  to  be  a  melancholia. 
This  outlook  is  apparently  much  brighter  than  that  taken  by  some  writers. 
It  is  perhaps  because  neurologists  see  cases  earlier  and  do  not  deal  greatly 
with  custodial  patients. 

Treatment. — The  treatment  of  psychasthenia  in  all  its  forms  is  essen- 
tially one  of  hygiene,  tonic  measures,  occupation,  restraint  and  peda- 
gogical training.  Without  such  measures  very  little  can  be  done;  but 
with  them  all  but  the  worst  cases  can  be  managed  with  fair  satisfaction. 
This  general  statement  applies  to  dipsomania  and  the  drug  habits,  as  well 
as  to  the  obsessions  and  the  morbid  fears  and  doubts.  It  is  as  useless  to 
treat  these  cases  (except  in  the  mildest  forms)  by  medication  and  at  home 
as  it  is  to  treat  the  drink  habit  or  the  major  hysterical  conditions.  There 
are  no  specific  drugs.     In  the  mild  types,  characterized  simply  by  fixed 


PSYCHASTHENIA  513 

ideas  and  a  certain  amount  of  fear  and  doubts,  hypnotic  treatment   is 
certainly  of  some  use.     This  apphes  especially  in  the  younger  cases. 

The  method  of  psycho-analysis  and  mental  catharsis,  of  hunting  for 
the  irritative  subconscious  complex,  and  explaining  the  mechanism  of 
the  obsession,  sometimes  cures,  sometimes  does  harm.  All  the  cases  thus 
cured  can  be  relieved  by  simpler  measures,  though  in  so  far  as  psycho- 
analysis means  pedagogics  and  re-education  it  is  exactly  in  line  with  the 
older  and  long  employed  therapeutics. 


33] 


CHAPTER  XXIII 
NEURASTHENIA  (NERVOUS  EXHAUSTION,  BEARD'S  DISEASE) 

The  condition  which  is  called  neurasthenia  is  often  only  an  exaggera- 
tion or  pathological  emphasis  of  a  neuropathic  constitution.  Persons 
of  a  highly  nervous  organization  often  have  at  various  times,  some 
symptoms  of  neurasthenia. 

Neurasthenia  is  a  functional  nervous  disorder,  characterized  by 
nervous  weakness  and  irritability,  so  that  the  patient  is  exhausted  by 
slight  exertions,  reacts  excessively  to  irritations  and  is  largely  or  entirely 
incapacitated  for  his  daily  tasks.  In  popular  usage,  neurasthenia  is  a  name 
often  given  to  what  is  really  some  serious  disorder  such  as  melancholia. 

Nervous  exhaustion  is  rarely  a  disorder  by  itself,  but  is  more  often  a 
condition  associated  with  some  morbid  mental  state. 

Besides  or  with  this  general  neurasthenic  condition  there  are  local 
neurasthenias,  affecting  especially  vasomotor,  gastric,  enteric  and 
sexual  functions. 

There  are  evidences  that  the  neuropathic  constitution  existed  in  all 
ages,  but  coherent  descriptions  of  clinical  types,  like  the  neurasthenia 
of  modern  days,  are  not  found  in  literature  until  the  past  century.  The 
credit  of  calling  attention  to  this  condition  most  insistently,  most  acutely, 
and  most  successfully  is  due  to  Dr.  George  M.  Beard,  though  he  described 
conditions  some  of  which  are  now  placed  in  other  groups.  The  evidence 
is  rather  conclusive  that  the  human  race  now  suffers  relatively  more  from 
nervous  irritability  and  exhaustion,  in  its  various  types,  than  it  did  in 
the  past.  We  find  also  that  neurasthenia  is  more  frequent  among  the 
partly  civilized  and  pioneer  races  such  as  that  of  the  United  States. 
One  sees  it  in  the  white  and  yellow  races,  but  not  in  the  brown  or  black. 
The  nervous  temperament  and  the  strenuous  activity  of  North  Americans 
are  said  to  be  due  in  part  to  the  waves  of  cold  air  which  pour  down  upon 
our  Western  and  Northwestern  States,  causing  quick  changes  of  tem- 
perature and  a  cool,  dry,  stimulating  climate.  Neurasthenia  prevails 
rather  more  in  dry  temperate  climates,  but  it  is  by  no  means  infrequent 
in  the  tropical  regions,  and  is  to  be  found  in  the  West  Indies  and  in  the 
republics  of  South  and  Central  America  in  its  classical  forms.  White 
people  living  in  the  tropics,  unless  under  the  best  sanitary  conditions, 
become  nervous,  and  Dr.  Woodruff  asserts  that  its  cause  is  the  excessive 
light  acting  upon  non-pigmented  skins.  Neurasthenia  is  found  rather 
more  often  in  men  than  in  women,  but  the  difference  is  not  great. 

514 


NEURASTHENIA  515 

The  neurasthenic  age  ranges  from  eighteen  to  fifty-five,  but  the 
larger  proportion  of  cases  is  met  with  between  the  years  of  twenty 
and  fifty.  Occasionally  symptoms  resembling  neurasthenia  may  be 
seen  in  children  of  the  age  of  twelve  or  thirteen,  and  occasionally  also 
there  develops  a  kind  of  senile  neurasthenia,  which  is,  however,  often 
associated  with  hypochondriasis,  and  some  definite  degenerative  changes 
in  the  nervous  or  vascular  system. 

In  men  neurasthenia  occurs  more  often  in  the  single;  in  women  the 
relation  is  somewhat  reversed,  so  that,  taking  both  classes,  the  married 
and  the  unmarried  are  about  equal. 

Neurasthenia  does  not  much  affect  the  people  of  the  country  and 
small  towns,  though  it  does  exist  there.  In  great  cities  the  number  of 
neurasthenic  women,  among  the  wives  of  laborers  and  artisans,  is  rather 
large,  and  this  is  the  natural  result  of  the  strain  of  living  with  husbands 
who  are  dissipated,  and  of  rearing  large  families  of  children  in  the  close 
quarters  of  a  tenement  house.  The  disease  is  relatively  more  frequent 
in  the  educated  classes. 

Hereditary  influence  plays  a  very  considerable  part  in  the  develop- 
ment of  neurasthenia.  We  can  usually  find  that  there  is  a  history  of 
migraine  or  some  nervous  irritability,  of  alcoholism  or  some  psychosis 
upon  one  side  or  the  other.  A  distinct  history  of  the  major  neuroses 
or  of  severe  mental  diseases  is  rare,  but  there  is  no  doubt  that  a  very  large 
proportion  of  neurasthenics  come  into  the  world  with  an  over-sensitive 
and  weakened  nervous  system.  They  may  be  strong  enough  to  undergo 
the  ordinary  strain  of  life,  but  break  down  under  some  specially  exciting 
cause. 

The  exciting  causes  of  neurasthenia  are  very  various,  but  they  can 
most  of  them  be  classed  under  the  head  of  excessive  mental  strain, 
shock,  sexual  abuse,  and  the  influences  of  exhausting  fevers,  of  chronic 
infections  like  syphilis,  and  of  excesses  in  alcohol. 

The  practice  of  masturbation  is  one  of  the  things  for  which  neu- 
rasthenics very  often  keenly  reproach  themselves  and  over  which  much 
hypochondriacal  brooding  develops.  Excesses  of  this  kind,  however, 
are  usually  a  sign  of  a  degenerative  or  unbalanced  nervous  system  rather 
than  a  cause.  The  actual  harm  done  is  greatly  exaggerated,  however 
strongly  this  practice  is  to  be  reprobated.  Excessive  and  unnatural 
indulgences,  such  as  sodomy,  coitus  interuptus,  etc.,  tend  to  weaken 
the  nervous  system  and  are  causal  factors  of  neurasthenia.  Bad  methods 
of  education  combined  with  excessive  study  may  lead  to  nervous  exhaus- 
tion. This  is  usually  seen  in  ambitious  students  who  are  forcing  their 
way  under  great  disadvantages  through  professional  schools  and  into 
professional  practice.  Young  women,  who  are  excessively  devoted  to 
social    indulgences,  sometimes  break    down  with    nervous    exhaustion. 


516  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  studies  and  training  of  the  primary  and  secondarj^  schools  may 
prepare  the  way  for  these  catastrophes,  but  thej'^  rarely  come  before  the 
eighteenth  year,  and  then  it  is  not  the  hard  work  of  schools  but  the  bad 
habits  of  life  at  the  period  of  education  which  break  down  the  student. 
Work  and  study  alone  do  not  cause  neurasthenia,  but  are  healthful 
except  to  certain  persons  who  are  of  bad  stock  and  are  destined  to  be 
neurasthenic  at  the  time  of  adolescence. 

Typical  attacks  of  neurasthenia  are  undoubtedly  brought  on  by 
the  fright  and  shock  incident  to  severe  injuries  or  exposure  to  great 
danger,  as  in  railroad  collisions  and  other  frightful  forms  of  accident. 
A  large  proportion  of  the  so-called  "traumatic  neuroses"  are  partly  forms 
of  neurasthenia ;  and  morbid  mental  states  can  in  time  induce  a  neurasthe- 
nia just  as  the  reverse  is  true.  Neurasthenia  can  be  brought  on  also  by 
excessive  child-bearing,  the  drain  of  lactation  and  domestic  trouble, 
great  excesses  in  eating  and  drinking,  and  the  strain  of  hard  domestic 
life  and  of  sickness  and  nursing.  Neurasthenia  sometimes  follows  an 
acute  infection  like  that  of  typhoid  fever  or  the  grippe.  It  may  also  be 
induced  by  the  infection  of  syphilis  (see  Luetic  Neurasthenia),  although 
this  must  not  be  confused  with  the  neurasthenic  symptoms  which  precede 
paresis  and  have  an  organic  basis. 

Much  weight  has  been  laid  upon  the  importance  of  eye-strain  in 
producing  neurasthenia,  and,  given  a  neuropathic  constitution,  there  is 
no  doubt  that  the  defect  in  the  refraction  of  the  eye  or  in  muscular 
equilibrium  may  cause,  or  at  least  keep  up,  a  neurasthenic  state.  The 
Same  is  probably  true  of  severe  forms  of  gastric  disturbance,  and  of 
disease  of  the  pelvic  organs,  such  as  subinvolution,  decided  displace- 
ments, and  chronic  ovaritis  or  salpingitis.  In  men  the  existence  of 
prostatic  irritation,  of  irritable  strictures,  and  hemorrhoids  and  fissures 
may  start  up  neurasthenic  symptoms. 

The  existence  in  neurasthenics  of  a  tendency  to  constipation,  or  what 
is  popularly  known  as  "biliousness,"  accompanied  by  a  gouty  or  lithsemic 
diathesis,  has  been  much  dwelt  upon,  and  at  one  time  neurasthenia  was 
thought  to  be  largely  the  expression  of  a  disturbed  state  of  the  metabolism 
— a  phase  only  of  gout  or  lithsemia.  This  tendency,  however,  is  rather 
the  result  of  the  weak  nerve-centres  than  the  cause,  though  the  two  often 
act  in  a  vicious  circle.  Prolonged  and  severe  dyspeptic  disturbances, 
especially  when  associated  with  atony  of  the  stomach  and  bowels  and 
the  condition  known  as  gastroptosis  and  enteroptosis,  are  exciting  or 
maintaining  causes.  Hyperthyroidism  and  defects  in  other  internal 
secretions  may  cause  neurasthenic  symptoms. 

I  would  sum  up  the  leading  causes  of  neurasthenia  thus: 

1.  Hereditary  nerve  instability. 

2.  Overwork  and  worry. 


NEURASTHENIA  517 

3.  Severe  shocks,  with  or  without  injury. 

4.  Infections. 

5.  Abuse  of  stimulants  and  narcotics. 

6.  Abuse  of  sexual  functions. 

7.  Disorder  of  digestive  functions,  autoxsemia  and  glandular  disturb- 
ances. On  the  whole,  the  causes  are  most  often  a  bad  heredity  and 
foolish  living. 

Symptoms. — The  symptoms  of  neurasthenia  are  relatively  definite, 
but  a  great  deal  of  what  is  mental  has  been  written  into  the  disorder. 
In  other  words,  the  minor  psychoses  such  as  hysteria,  psychasthenia, 
hypochondria,  abortive  melancholia  have  been  often  looked  upon  as 
neurasthenia.  The  time  has  come  now,  however,  when  these  conditions 
should  be  recognized  and  treated  separately,  and  thus  greatly  limit  the 
field  of  the  disease.  For  neurasthenia  is,  strictly  speaking,  the  name  to 
be  applied  only  to  a  neurosis — a  morbid  nervous,  not  a  morbid  mental, 
state. 

It  will  be  easier  to  understand  what  neurasthenia  is  by  indicating 
first  what  it  is  not;  in  other  words,  by  excluding  certain  quite  well- 
known  groups  of  psychic  disorders. 

First,  then,  we  exclude  from  the  symptomatology  of  neurasthenia 
the  mild  types  of  recurrent  melancholia  or,  as  they  are  now  termed, 
"the  depressive  phase  of  manic-depressive  insanity."  Second,  we  ex- 
clude the  psychosis  characterized  by  a  dominant  sensory  complex. 
It  includes  patients  who  are  continually  complaining  of  dysthesias, 
headaches  and  head  parsesthesias,  stomach  troubles  and  various  bizarre 
forms  of  physical  suffering  and  functional  disturbance.  The  dis- 
ease is  seen  in  young  people  and  it  is  only  an  abortive  or  early 
type  of  the  melancholia  of  involution.  It  is  sometimes  called  anxiety 
psychosis.  Third,  we  exclude  the  psychosis  (psychasthenia)  character- 
ized by  obsessions  and  fixed  ideas,  of  apprehensions,  panics  of  doubts, 
abulic  states,  and  psychic  tics. 

Thus  we  remove  from  the  realm  of  neurasthenia  all  the  pure  psychoses. 
These  psychoses  in  mild  and  abortive  types  give  many  of  the  symptoms 
of  neurasthenia,  because  they  usually  have  a  neurasthenic  basis. 

Under  the  head  of  neurasthenia  proper  there  are  two  types  of  a 
neurosis,  one  neurasthenia  prgecox  or  neurasthenia  of  adolescence,  and 
second,  the  neurasthenia  acquisita  or  the  neurasthenia  produced  generally 
later  in  life  by  Avork,  worry,  shock,  infections,  toxins,  sexual  excesses, 
and  other  causes  already  named.  Besides  these  two  types,  or  associated 
with  them,  we  find  local  neurasthenias,  affecting  especially  the  heart, 
vasomotor  centres,  digestive  or  sexual  organs. 

The  general  symptoms  of  primary  neurasthenia  are  very  much 
like  those  of  the  acquired  type,  and  the  following  description  fairly  out- 


518  DISEASES    OF    THE    NEEVOUS    SYSTEM 

lines  the  clinical  picture  of  each.  In  the  prsecox  type,  the  asthenia  is 
of  a  more  simple  character;  there  is  less  evident  trouble  with  special 
organs,  less  mental  distress  and  fewer  psychic  symptoms.  The  young 
person  gives  out  all  along  the  line,  but  the  malady  is  apt  to  be  more 
persistent,  and  after  apparent  cure  remissions  may  occur.  It  is  not  a 
frequent  disorder,  and  it  may  come  on  long  after  the  ordinary  period, 
which  is  about  the  eighteenth  to  the  twenty-fifth  years.  Whenever  this 
type  of  neurasthenia  is  followed  by  a  serious  psychosis,  such  as  melan- 
cholia, we  may  infer  that  the  original  attack  was  really  a  mild  psychosis. 

One  of  the  first  symptoms  is  an  annoying  insomnia.  It  is  usually 
an  early  insomnia,  i.e.,  the  patient  cannot  get  to  sleep  till  late,  and  then 
sleeps  badly,  frequently  awakening.  Distressing  dreams  occur,  and  the 
patient  wakes  unrested  and  more  tired  than  when  he  went  to  bed.  The 
patient  complains  of  a  general  feeling  of  mental  depression.  He  can 
work,  but  soon  gets  tired.  He  can  play  but  it  exhausts  him  so  that  he 
cannot  sleep  or  has  a  headache.  All  mental  and  physical  effort  has  to  be 
paid  for  by  periods  of  rest.  He  wants  to  work  and  to  play  but  he  cannot. 
He  is  easily  irritated  at  things  which  before  caused  him  no  annoyance, 
and  becomes  a  source  of  domestic  unrest  and  unhappiness.  He  suffers 
from  a  number  of  peculiar  sensations  which  are  called  "cephalic  parsesthe- 
siae."  These  are  sensations  of  pressure  on  the  top  of  the  head,  or  a 
feeling  of  constriction  around  the  temples,  or  a  burning  spot  on  the 
vertex,  or  tenderness  of  the  scalp.  Sometimes  he  has  a  sense  of  weak- 
ness or  even  pain  in  the  back  of  the  neck.  All  these  things  are  increased 
by  the  use  of  the  mind  or  by  bodily  exertion,  and  they  are  all  more 
common  in  the  acquired  types.  Headache  occurs  in  perhaps  one-half 
of  the  cases,  the  headache  being  usually  either  frontal  or  occipital;  or  both. 
It  is  often  very  persistent,  and  in  fact  a  chronic  headache,  not  due  to 
tumor  or  meningitis  or  syphilis,  is  almost  invariably  of  neurasthenic 
origin.  This  neurasthenic  headache  is  usually  diurnal  only,  coming  on 
in  the  morning  when  the  patient  wakes  up  and  lasting  a  good  part  of 
the  day.  It  does  not  often  keep  him  awake  at  night.  In  this  point 
it  is  distinguished  from  the  headaches  of  syphilis  and  of  meningitis  or  of 
tumors.  Women  suffer  from  these  headaches,  and  from  pains  in  general, 
more  often  than  men.  They  in  particular  have  much  pain  in  the  back 
of  the  neck  and  along  the  spine.  This  keeps  them  from  walking  or 
being  upon  their  feet,  and  it  may  develop  into  a  form  of  trouble  known 
as  ''spinal  irritation." 

The  special  senses  are  functionally  affected.  The  patients  can  often 
see  quite  well,  but  their  eyes  soon  tire;  they  cannot  read  a  book  long 
because  it  makes  the  eyes  smart  or  produces  some  headache.  Examina- 
tions of  the  neurasthenic's  eye  frequently  show  the  existence  of  some 
refractive  error,  most   frequently  astigmatism  and  hypermetropia;  de- 


NEURASTHENIA  519 

fects  in  the  ocular  muscles,  and  especially  weakness  of  the  internal  recti, 
often  occur.  Patients  have  frequently  complained  to  me  of  a  defect  in 
visual  memory.  They  see  a  thing  or  face  but  do  not  remember  it  again 
as  readily  as  they  used  to.  There  is  no  limitation  of  the  visual  field  in 
true  neurasthenia  uncomplicated  by  organic  disease,  but  there  is  a  morbid 
susceptibility  to  fatigue,  particularly  of  the  periphery  of  the  vision,  so  that 
after  long  testing,  objects  in  the  periphery  becomes  less  distinct,  and  a 
sort  of  artificial  limitation  of  the  field  may  be  produced.  In  some  cases 
an  object  which  is  brought  from  without  into  and  across  the  visual  field 
is  seen  in  wider  range  than  an  object  which  is  placed  in  the  centre  of 
vision  and  carried  gradually  out  toward  the  periphery.  This  is  the  re- 
verse of  the  normal  condition,  and  is  known  as  "Foerster's  shifting  type." 
A  slight  drooping  of  the  lids,  and  excessive  mobility  of  the  iris  have  been 
noted  in  neurasthenia. 

Neurasthenics  of  the  acquired  type  sometimes  suffer  from  tinnitus, 
which  is  very  distressing  and  aggravates  every  other  nervous  symptom, 
but  this  usually  occurs  only  in  connection  with  actual  disease  of  the 
middle  ear,  or  in  old  people  with  degenerative  changes  in  the  cerebral 
blood-vessels.  An  excessive  sensibility  to  noises,  and  even  the  pleasant 
sounds,  like  those  of  music,  may  be  present.  Neurasthenics  sometimes 
cannot  bear  even  the  most  enchanting  melodies.  A  similar  morbid 
sensibility  to  taste  and  smell  may  be  present.  But  these  are  matters  of 
minor  moment  and  are  due  to  temperamental  or  psychic  complications. 

In  neurasthenia  the  general  muscular  strength  is  lessened  and  easily 
exhausted  although  the  patient  may  not  have  any  actual  atrophy. 

The  cutaneous  and  deep  reflexes  are  generally  exaggerated.  These 
conditions  vary  considerably,  however,  in  different  cases,  and  are  more 
marked  in  the  younger  patients  and  those  of  a  neuropathic  constitution. 

The  sexual  function  is  irritable  and  weak  and  in  certain  cases  this  local 
trouble  dominates  the  situation.  But  here  a  psychosis  is  often  complicat- 
ing the  neurasthenia. 

There  is  a  considerable  disturbance  of  the  heart  function  in  neuras- 
thenia. The  most  frequent  condition  is  an  acceleration  of  the  pulse 
beat  from  very  slight  cause.  A  pressure  over  some  painful  point  in  the 
body  will  sometimes  bring  up  the  pulse  from  80  to  90  to  over  100,  and  it 
will  remain  there  for  one  or  two  minutes.  This  is  called  ''Rumpf's 
symptom."  Arhythmia  and  palpitation  of  the  heart  are  less  frequently 
observed.  Cardiac  weakness  is  an  important  condition  in  many  forms 
of  neurasthenia  and  underlies  many  of  the  asthenic  symptoms.  This  is 
particularly  true  of  the  neurasthenias  of  more  advanced  life.  The  blood- 
pressure  is  usually  low.  There  is  an  abnormal  difference  between  the 
pulse-rate  and  pressure  in  the  vertical  and  horizontal  positions  (Crampton 
test). 


520  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  existence  of  some  degree  of  thyroidism  should  be  looked  out  for 
in  patients  with  very  irritable  hearts.  Ordinary  valvular  lesions  have 
little  to  do  with  causing  neurasthenia,  but  when  a  patient  with  a  bad 
myocardium  becomes  neurasthenic  his  heart  gives  him  much  trouble. 
He  feels  its  irregular  beating  and  skipping  and  he  hears  its  throb  when  he 
lies  on  his  pillows;  its  action  is  disturbed  by  very  slight  exertion  and  slight 
anginal  sensations  are  present. 

A  great  deal  of  emphasis  has  been  laid  upon  the  vasomotor  disturb- 
ances of  neurasthenia.  The  most  common  symptoms  are  those  due  to 
weak  and  irritable  vasomotor  centres,  viz.,  cold  hands  and  feet,  flushings, 
pallor,  poor  reaction  to  the  cold  of  the  air  or  the  bath.  Vago-tonic  and 
sympathetico-tonic  seizures  are  more  common  in  psychasthenia. 

Many  of  the  symptoms  which  we  now  call  "neurasthenic"  were  de- 
scribed by  Dr.  Prout  and  Dr.  Golding  Bird  early  in  the  last  century  and 
were  held  by  these  gentlemen  to  be  due  to  oxaluria.  This  was  a  condition 
characterized  by  flatulent  dyspepsia,  melancholia,  and  nervous  irritability 
and  was  thought  to  be  due  to  defective  metabolism,  resulting  in  the  pro- 
duction of  an  excess  of  oxalic  acid.  As  a  matter  of  fact  the  condition  of 
the  urine  is  of  not  much  importance  in  the  symptomatology  of  neuras- 
thenia, except  in  so  far  as  it  indicates  an  autotoxsemia,  or  a  deficient  ex- 
cretion of  nitrogenous  bodies,  or  evidences  of  slowed  or  quickened 
metabolism. 

The  urine  of  neurasthenia  is  variable  in  specific  gravity,  but,  on  the 
whole  rather  low ;  and  the  daily  amount  is  below  the  average.  The  func- 
tional acitivity  of  the  kidney  may  be  lowered  and  the  blood  in  patients 
with  complicating  cardio-renal  disorder  should  be  tested  for  abnormal 
nitrogenous  constituents  and  for  sugar,  urinary  examinations  not  being 
always  sufficient. 

The  digestion  of  neurasthenics  is  usually  affected,  and  a  large  propor- 
tion of  them  are  probably  treated  mainly  for  their  stomach  conditions. 
The  neurasthenic  has  a  feeble  digestion,  the  gastric  juice  being  deficient 
in  acid  and  the  gastro-intestinal  motility  slow.  In  a  certain  number  a 
gastroptosis  occurs,  and  the  lower  curvature  drops  below  the  umbilicus. 
The  patient  suffers  from  flatulence,  acidity  and  epigastric  discomfort, 
with  anorexia  and  nervousness.  There  is  atony  of  the  gastric  wall,  but 
no  very  marked  change  in  secretion,  and  no  especial  fermentation 
(Lockwood).  It  is  only  in  patients  who  have  abused  themselves  with 
alcohol  or  tobacco,  or  excessive  indulgence  in  sweets,  or  with  ravenous 
feeding  that  worse  conditions  are  found.  In  people  of  more  advanced 
age,  feebleness  of  digestion  is  often  associated  with  a  more  serious  relaxa- 
tion of  the  stomach  and  intestinal  walls,  and  a  great  deal  of  atony  of  the 
whole  intestinal  tract,  with  patency  of  the  iliocaecal  valve.  In  these 
cases,  which  we  find  particularly  often  in  women,  the  prolpase  of  the  in- 


NEURASTHENIA  521 

testines,  stomach,  and  perhaps  of  a  kidney  may  cause  a  great  many  dis- 
tressing symptoms.  The  condition  has  been  described  by  Glenard  under 
the  name  of  "enteroptosis,"  and  it  undoubtedly  is  an  important  factor 
in  keeping  up  the  neurasthenia  of  some  women  in  adult  and  middle  life. 

Its  investigation  has  been  much  helped  of  late  by  bismuth  feeding  and 
X-ray  photographs,  and  in  all  persistent  neurasthenias  with  intestinal 
symptoms  there  should  be  a  thorough  study  of  the  secretory,  muscular 
and  anatomical  conditions  of  the  gastro-intestinal  tract. 

Among  the  most  serious,  though  fortunately  rare,  symptoms  of 
neurasthenia  involving  the  digestive  tract  is  the  condition  known  as 
"mucous"  enteritis.  This  trouble  generally  attacks  women  rather 
than  men,  and  usually  women  between  the  ages  of  twenty-five  and 
forty.  It  comes  on  after  the  patient  has  become  exhausted  by  pro- 
longed domestic  cares  or  fashionable  dissipation,  or  some  shock. 
It  is  one  of  the  earlier  symptoms  of  the  nervous  weakness,  and  begins 
with  abdominal  pain,  followed  by  attacks  of  diarrhcBa,  in  which  tubular 
casts  are  passed,  or  portions  of  such.  This  diarrhoea  is  painful,  colicky, 
and  alternates  with  periods  of  constipation.  There  is  a  somewhat 
spastic  condition  of  the  bowel,  as  though  it  were  irritated  and  closed  down 
upon  the  contents  of  the  intestine.  The  term  mucous  enteritis  is  not 
strictly  a  proper  one,  since  microscopical  examinations  and  autopsical 
reports  show  that  the  substances  thrown  off  are  not  mucous  mainly  and 
that  there  is  no  actual  inflammation.  The  casts  that  are  found  in  the 
stools  are  composed  principally  of  albuminous  substances,  the  product 
apparently  of  the  decomposition  or  disintegration  of  the  epithelial  cells 
of  the  intestinal  walls.  While  mucous  enteritis  sometimes  occurs  in 
persons  who  are  profoundly  asthenic  without  any  decided  neurasthenia, 
yet,  in  the  great  majority  of  cases,  it  is  a  symptom  of  neurasthenia,  and 
can  be  successfully  treated  only  on  such  a  basis. 

The  respirations  in  neurasthenia  are  generally  normal,  but  shallow 
and  deficient  respiratory  expansion  sometimes  exists.  In  women  par- 
ticularly I  have  often  found  that  there  was  an  actual  inability  properly 
to  expand  the  chest  and  inflate  the  lungs. 

The  temperature  is  normal,  and  a  very  variable  temperature  of  the 
skin  is  simply  dependent  upon  vasomotor  instability. 

The  composition  of  the  blood  is  often  quite  normal.  Hosslin  finds 
that  even  in  those  patients  who  appear  to  be  anaemic  there  is  a  normal 
amount  of  haemoglobin;  however,  anaemia  certainly  exists  in  many  cases, 
and  there  is  no  question  that  the  use  of  iron  is  often  of  great  benefit. 

Variations  in  the  weight  of  the  neurotic  often  occur.  Neurotic  pa- 
tients may  gain  or  lose  ten  or  twenty  pounds  within  a  few  months.  The 
secretions  of  the  skin  are  usually  increased,  and  the  patient  sweats  easily 
and  profusely.     In  other  cases  of  a  less  irritative  type  the  skin  is  inclined 


522  DISEASES    OF   THE    NERVOUS    SYSTEM 

to  be  dry.  Its  nutritional  condition  is  poor,  the  hair  falls,  and,  according 
to  Beard,  there  is  a  tendency  to  early  decay  of  the  teeth. 

Traumatic  Neurasthenia,  Traumatic  Psycho-neurosis. — This  condi- 
tion is  nothing  else  than  neurasthenia  with  a  more  than  ordinary  mental 
element  of  anxious  receptiveness  to  physical  impressions.  The  following 
description  is  in  a  degree  a  repetition,  but  it  is  given  here  as  it  is  very 
nearly  the  actual  record  of  a  typical  case. 

The  patient  is  in  an  accident  and  has  suffered  from  some  physical 
injury,  and  great  mental  shock.  He  is  perhaps  helped  to  his  home,  and 
his  sprains  or  bruises  attended  to.  He  goes  to  bed  and  sleeps;  he  wakes 
up  the  next  morning  feeling  not  quite  so  well  as  usual,  but  congratulating 
himself,  perhaps,  on  having  gotten  off  so  easily.  He  resumes  his  work 
and  finds  that  he  can  do  it,  though  with  not  quite  so  much  ease  as  usual 
and  he  very  likely  suffers  from  some  pain  due  to  a  strain  or  bruise  that  he 
has  received.  In  a  few  days — almost  always  within  a  week — he  begins 
to  notice  that  he  is  more  nervous  than  usual,  that  little  things  irritate 
him  which  did  not  do  so  before,  that  his  head  seems  somewhat  confused, 
and  that  the  effort  to  work  is  wearying.  His  sleep  is  disturbed,  and  he 
wakes  up  in  the  morning  unrefreshed  by  his  night's  repose.  He  becomes 
somewhat  despondent  over  his  condition,  and  thoughts  of  paralysis  or 
some  other  serious  ailment  annoy  him.  His  head  aches,  the  pain  being 
more  or  less  constant  and  diffused,  and  located  usually  over  the  forehead 
or  at  the  back  of  the  neck.  He  has  unpleasant  sensations  in  the  head, 
such  as  that  of  constriction  or  pressure  or  scalding  feelings.  His  back  also 
is  continually  painful,  and  walking  increases  it.  His  nervousness  be- 
comes more  marked,  and  close  examination  shows  a  little,  fine  tremor  in 
the  hands.  He  has  also  sometimes  creeping  sensations  over  the  body 
or  numb  feelings  in  the  extremities.  He  tires  very  easily.  He  is  emo- 
tional, and  becomes  more  despondent  as  the  days  go  on.  Sometimes 
he  has  spots  before  his  eyes,  noises  in  his  head,  or  ringing  in  the  ears. 
Reading  is  laborious  and  increases  his  headache;  so  also  does  attention 
to  work.  His  appetite  becomes  capricious  and  his  bowels  are  consti- 
pated. He  suffers  somewhat  from  flatulency  and  dyspepsia.  His  heart 
palpitates  easily,  and  the  pulse  is  a  little  accelerated.  Sometimes  for  a 
few  days  there  is  a  little  weakness  about  the  bladder  or  irritability  of 
that  viscus.  His  sexual  power  is  diminished.  His  blood  pressure  is 
lower  than  normal.  Very  slight  excitement  produces  sweating  of  the 
hands  or  coldness  of  the  extremities.  He  loses  a  little  flesh.  The  picture, 
as  may  be  seen,  is  very  much  like  that  of  neurasthenia  of  the  acquired 
type  plus  a  little  more  of  the  physical  and  sensory  complex. 

These  symptoms  may  be  several  weeks  in  developing,  and  during  this 
time  he  may  perhaps  consult  a  lawyer  about  his  case.  If  so,  the  anxieties 
of  litigation  begin  to  add  to  and  intensify  his  troubles.     He  consults  a 


NEURASTHENIA  523 

physician,  and  the  physician  finds  the  subjective  symptoms  that  I  have 
mentioned.  Objectively,  when  examined,  the  physician  will  discover 
that  the  muscular  power  is  somewhat  weakened,  that  there  is  a  certain 
amount  of  the  fine  tremor  perhaps  in  his  hands.  The  knee-jerks  and 
elbow-jerks  are  exaggerated;  there  are  tender  points  along  the  spine  and 
upon  the  head.  In  making  him  stand  with  his  eyes  closed  there  is  a  cer- 
tain amount  of  static  ataxia  discovered.  The  pupils  are  often  dilated 
and  mobile,  and  examination  of  the  visual  field  shows  sometimes  a  slight 
contraction,  at  other  times  the  "shifting  type"  already  described.  In 
many  cases  a  degree  of  peripheral  retinal  anaesthesia  will  be  discovered. 
The  pulse  will  be  found  accelerated,  and  pressure  on  a  tender  point  may 
send  it  up  very  rapidly;  a  slight  exertion  will  also  accelerate  it.  There 
will  be  something  apparent  in  the  physiognomy  of  the  case  which  shows 
the  man  to  be  in  a  nervous  and  asthenic  condition.  Sometimes  the  pains 
from  which  the  patient  suffers  in  the  back  and  the  weariness  in  the  limbs 
are  so  great  that  he  remains  a  good  deal  of  the  time  in  bed.  In  all  cases 
he  will  assert  most  positively  that  he  is  unable  to  work  or  to  take  that 
interest  in  his  affairs  that  he  has  previously  done.  In  a  good  many  cases 
there  will  be  added  to  the  foregoing  picture  a  number  of  symptoms  due 
to  some  local  injury;  for  example,  the  arm  may  have  been  wrenched  or 
bruised,  and  the  result  may  be  a  certain  amount  of  neuritis  and  weakness 
or  pain  in  that  member;  in  other  cases  the  back  may  have  been  so  severely 
sprained  that  the  typical  symptoms  of  spinal  irritation  ensue,  and  this  is 
particularly  apt  to  be  the  case  when  women  are  injured;  in  other  cases, 
again,  the  legs  may  have  been  hurt  to  such  an  extent  that  a  sciatica  or 
some  other  form  of  neuralgia  develops. 

The  foregoing  symptoms,  varying  in  amount  and  degree,  will  last, 
with  little  change,  for  a  very  long  period  of  time.  If  the  case  goes  into 
litigation,  there  is  added  the  worriment  occasioned  by  having  to  go 
through  the  disturbing  experiences  of  trial  by  jury  so  that  what  was  at 
first  mainly  a  neurosis  becomes  a  psycho-neurosis,  or  almost  a  psychosis. 
In  many  cases,  after  the  trial  has  been  settled  and  damages  awarded  or 
otherwise,  the  patient  begins  to  mend,  and  in  a  certain  proportion  of  cases 
he  gets  completely  well.     This  is  not  invariably  the  rule. 

Spinal  Irritation  (Spinal  Psycho -neurosis). — Spinal  irritation  is  a 
form  of  neurasthenia  in  which,  associated  with  the  general  neurasthenic 
symptoms,  are  certain  special,  painful  symptoms,  related  chiefly  to  the 
sensory  nerves  of  the  spine.  These  cases  have  in  the  past  been  described 
under  the  head  of  "spinal  anaemia"  and  "hypersemia."  They  may  de- 
velop in  traumatic  neurasthenia.  The  patients  are  usually  young  women, 
between  the  ages  of  sixteen  and  twenty-five.  The  trouble  is  sometimes 
brought  on  by  injuries  or  by  a  physical  over-strain.  Sometimes  it  seems 
to  be  associated  with  a  natural  weakness  of  the  spinal  muscles  and  a 


524  DISEASES    OF    THE    NERVOUS    SYSTEM 

consequent  curvature.  Sometimes  it  follows  acute  infectious  diseases. 
The  patient  begins  by  complaining  of  pain  in  the  back — usually  in  the 
lower  part — and  also  in  the  back  of  the  neck.  These  pains  occur  on 
standing  or  walking,  or  any  exertion,  and  are  so  severe  that  the  patients, 
in  the  course  of  a  few  weeks  or  months,  give  up  attempting  to  walk  about. 
They  get  relief  and  comfort  in  bed,  and  so  they  go  there  and  remain. 
The  pains  are  of  a  heavy,  aching  character,  increased  until  they  become 
very  sharp  when  attempts  at  movement  of  the  trunk  are  made.  There 
is  a  great  deal  of  tenderness  to  pressure  along  the  spinal  processes,  some 
of  these  processes  being  much  more  sensitive  than  others.  The  most 
sensitive  points  are  usually  in  the  back  of  the  neck  and  the  upper  dorsal 
vertebrae,  and  down  in  the  lumbar  region.  There  is  some  pain  also  upon 
pressure  alongside  of  the  spinal  processes.  Painful  points  often  vary, 
and  even  in  a  single  examination  the  patient  may  complain,  and  complain 
honestly,  of  different  sensitive  vertebrae.  Pressure  on  these  points  does  not 
often  bring  out  visceral  symptoms,  as  the  brothers  Grifhn  taught,  but  may 
cause  faintness,  nausea  and  tears  from  the  pain.  The  patients  suffer 
much  from  headaches.  The  arms  are  often  weak,  so  that  attempting 
to  sew  or  write  or  hold  a  book  causes  pain  in  the  neck  and  shoulders. 
The  legs  are  also  weak  and  the  circulation  is  poor.  There  is  sometimes 
palpitation  of  the  heart  and  precordial  distress.  A  certain  amount  of 
dyspepsia  is  always  present,  and  constipation  is  the  rule.  The  patients 
often  have  attacks  of  vomiting,  and  attempts  to  feed  them  require  much 
care.  The  menstrual  functions  become  irregular.  The  patient  grows 
weaker  and  often  becomes  bedridden,  especially  if  little  attempt  is  made 
to  overcome  the  symptoms  by  voluntary  effort  and  attention  to  nutri- 
tion. These  patients  generally  get  well  in  from  one  to  three  years,  but 
occasionally  they  sink  into  permanent  invalidism.  The  symptoms  are 
quite  as  much  due  to  mental  sensitiveness  and  disordered  cerebrum  as  to 
any  local  spinal  trouble,  and  the  term  psj'^cho-neurosis  is  a  more  correct 
one. 

Local  Neurasthenia. — There  are  cases  in  which  the  specially  weak 
and  exhausted  function  is  the  heart  and  vasomotor  centres,  or  the 
stomach  and  intestinal  tract,  or  the  sexual  organs.  The  symptoms 
here  are  much  the  same  locally  as  those  described  above  under  the 
head  of  neurasthenia.  But  the  patient  with  a  nervously  weak  stomach 
or  heart  or  sexual  organs  may  yet  be  strong  enough  to  do  a  fair  amount  of 
work.  It  is  only  one  or  two  of  the  somatic  functions  that  are  involved. 
Here  the  term  local  neurasthenia  is  a  justifiable  one.  In  many  of  these 
cases,  however,  a  mental  element  develops  and  often  local  neurasthenias 
are  also  associated  with  a  psychosis. 

Angiopathic  Neurasthenia. — Here  the  patient  has  some  general 
symptoms  of  neurasthenia,  but  in  particular  he  has  special  symptoms 


NEUEASTHENIA  525 

which  consist  of  a  sense  of  pulsation  or  beating,  which  involves  the 
whole  body.  The  tension  of  the  pulse  is  low,  the  rate  normal  or  slightly 
accelerated.  He  does  not  have  palpitations  of  the  heart,  as  in  Basedow's 
disease,  and  there  is  no  particular  dyspnoea  on  exertion.  The  skin  usually 
shows  a  striking  degree  of  dermography,  and  there  is  an  epigastric 
pulsation,  as  well  as  pulsation  of  the  carotid.  The  pathology  is  suggested 
by  the  fact  that  one  of  my  patients  was  rather  promptly  cured  by 
adrenalin.  And  the  trouble  may  be  due  to  an  inadequate  activity  of 
the  suprarenal  capsules. 

Neurasthenia  Gravis. — In  instances  which  are  fortunately  very 
rare  neurasthenia  assumes  a  very  severe  and  serious  type  of  exhaustion. 
The  patients  suffer  from  the  typical  symptoms  in  much  the  ordinary 
way,  but  the  degree  of  weakness  is  very  much  exaggerated.  Such 
patients  have  not  only  headaches  and  disturbed  sleep,  pains  in  the  back 
and  parsesthesise,  digestive  disturbances,  and  mental  depression,  but 
they  speedily  emaciate  to  a  considerable  extent.  They  take  food  in  fair 
amounts,  but  it  gives  them  no  strength.  The  most  careful  applications 
of  the  "rest  cure"  secure  for  them  only  temporary  benefit.  They  cannot 
walk  far  without  intense  fatigue  and  exhaustion,  with  subsequently  severe 
headaches,  or  even  attacks  of  vomiting  and  diarrhoea.  Despite  closest 
examination,  no  distinct  signs  of  organic  disease  can  be  discovered,  and 
I  have  known  such  patients  to  go  on  into  an  invalidism  which  has  lasted 
for  over  eight  years  with  final  recovery.  In  these  cases  there  is  not  an 
hysterical  or  even  large  hypochondriacal  element.  No  amount  of  sug- 
gestion or  "mind  cure"  has  much  effect  upon  them.  They  are  not,  in 
other  words,  hysterical,  bedridden  women,  but  often  men  who  have 
reached  or  passed  the  middle  period  of  life.  Even  these  very  worst  cases 
may  get  well. 

Pathogeny  and  Pathology. — Victims  of  neurasthenia  are  persons 
who  in  all  cases  have  either  inherited  or  acquired  a  nervous  system  with 
lessened  power  for  active  functioning.  There  probably  underlies  in 
neurasthenia  an  impaired  metabolic  power.  The  nerve-cells  break  down 
too  easily  and  build  up  too  slowly.  This  defect  is  partly  inherited,  but  is 
brought  out  in  the  struggles  of  maturer  life.  Glandular  defects  (thyroid, 
adrenals)  may  pronote  the  trouble  and  so  may  disorders  of  the  autonomic 
system  and  the  vasomotor  centres.  There  may  be  cases  of  pseudo- 
neurasthenia  in  which  the  exhaustions  and  irritations  are  psychogenous. 
Neurasthenia  then  becomes  a  symptom  of  hysteria. 

Diagnosis. — The  characteristic  of  neurasthenia  is  the  easy  exhausti- 
bility  after  mental  or  bodily  effort,  and  the  punishment  that  follows 
exertion.  The  mind  is  usually  alert,  there  is  no  profound  depression, 
and  thought  is  not  difficult  or  sluggish  at  first.  There  is  some  constitu- 
tional and  usually  some  physical  cause  for  the  condition.     In  all  these 


526  DISEASES    OF   THE    NERVOUS    SYSTEM 

ways  it  differs  from  the  mild  abortive  melancholias  with  which  it  is 
oftenest  confused.  The  feelings  of  anxiety  and  depression,  the  self- 
concern  are  not  in  great  excess  of  normal. 

The  so-called  "anxiety  nem'osis"  is  not  a  form  of  actual  neurasthenia, 
but  an  abortive  form  of  hypochondriacal  melancholia.  There  can  be  no 
question  of  this  fact,  and  the  attempt  to  erect  it  into  a  special  disease  is 
caused  by  insufficient  experience.  I  have  seen  many  cases  who  had 
attacks  of  this  so-called  malady  when  young  develop  true  melancholia 
of  involution  later.  The  neurasthenic  has  no  undue  alarm,  he  does  not 
tell  his  story  with  the  voluble  iterations  of  the  anxious  neurotic;  if  he 
does,  there  is  a  psychosis  imposed  on  the  neural  exhaustion. 

The  beginnings  of  dementia  prsecox,  mild  types  of  confusional  and 
exhaustion  psychoses,  early  paresis,  hysteria,  psychasthenia,  and  malinger- 
ing are  the  other  conditions  which  must  be  noted  in  making  a  diagnosis. 
The  diagnostic  criteria  are  given  under  the  description  of  these  disorders. 

The  diagnosis  of  the  cause  involves  a  thoroughgoing  study  of  the 
bodily  condition,  an  examination  for  reflex  irritations,  for  toxaemias,  for 
bad  environmental  conditions  and  bad  mental  training  and  habits. 

A  patient  may  be  suffering  from  a  number  of  bodily  ailments,  and  if 
this  person  be  at  the  same  time  of  a  somewhat  nervous  constitution  the 
condition  may  resemble  neurasthenia.  Those  persons  having  a  very 
feeble  digestion,  with  dilated  stomach  and  an  atonic  condition  of  the  ali- 
mentary tract,  may  get  depressed,  fretful,  and  sleepless;  so  a  person 
suffering  from  some  chronic  uterine  or  ovarian  or  bladder  trouble  may 
present  many  symptoms  of  nervous  irritation.  These  patients  may  have 
only  a  local  neurasthenia  or  a  real  local  disease  with  neurasthenia  as 
a  reflex  condition.  It  must  depend  largely  upon  the  good  sense  of  the 
physician  to  measure  the  importance  of  the  local  troubles  as  compared 
with  those  of  the  general  symptoms.  I  believe  that  the  fully  devel- 
oped type  of  neurasthenia  is  rarely  brought  out  by  local  disease  alone. 
Still,  I  have  seen  cases  with  neurasthenic  symptoms  cured  for  a  time  by 
washing  out  the  stomach,  and  enormous  relief  to  the  nervous  irritation 
to  result  from  treating  the  condition  of  the  blood  or  relieving  the  uterine 
disturbances. 

It  should  finally  be  remembered  that  some  neurasthenia  usually 
complicates  the  minor  psychoses. 

Course  and  Prognosis. — There  is  such  a  thing  as  acute  neurasthenia. 
This  follows  prolonged  debauches  and  long  periods  of  excessive  mental 
strain,  with  loss  of  sleep.  Such  patients  may  present  all  the  signs  of  neu- 
rasthenia, and  get  perfectly  well  in  two  or  three  weeks.  Neurasthenia, 
however,  is  essentially  a  chronic  disease,  and  when  speaking  of  it  we  refer 
to  this  type  of  the  disorder.  It  is  a  disease  which  comes  on  as  a  rule 
gradually,  developing,  however,  in  the  course  of  a  few  months.     It  may, 


NEURASTHENIA  527 

however,  come  on  suddenly  after  shocks  and  accidents,  and  it  may  de- 
velop or  follow  rapidly  after  an  acute  infectious  fever.  It  always  reaches 
its  height  in  a  comparatively  short  time,  and  runs  a  course  lasting  from 
one  or  two  to  seven  or  eight  years.  This  course  is  a  varying  one,  and  this 
variation  is  particularly  noticeable  when  the  patient  begins  to  get  well. 
The  patient  continues  to  improve  for  a  time  and  then  suddenly  falls  back, 
then  goes  forward  again,  and  thus  convalescence  progresses.  Complete 
restoration  to  health  is  possible  and  frequent,  but  the  patient  always  has 
to  take  more  care  of  himself  than  before.  As  a  result  of  an  attack  of 
neurasthenia,  men  and  women  who  have  suffered  from  it  are  apt  there- 
after to  lead  very  saint-like  and  ascetic  lives,  and  hence  they  as  a  rule 
live  long.  It  used  to  be  said  by  Dr.  Beard  that  neurasthenics  would 
have  a  long  and  happy  old  age.  They  pass  through  the  valley  of  the 
shadow  of  death,  but  the  experience  may  be  a  profitable,  if  not  a  pleasant 
one. 

Neurasthenia  prsecox  has  a  much  more  serious  prognosis,  especially 
as  regards  duration.  This  is  the  kind  that  may  last  seven  or  eight  years, 
but  recovery  usually  occurs.  Acquired  neurasthenia  often  lasts  only 
from  six  months  to  two  years.  Local  neurasthenias  are  also  curable, 
except  the  sexual  type,  which  is  an  obstinate  affection  if  it  is  a  purely 
neurasthenic  one. 

Treatment. — Naturally,  a  measure  of  leading  importance  in  the 
treatment  of  neurasthenia  is  rest,  and  the  problem  of  how  this  can  be 
obtained  is  the  first  one  to  confront  the  physician. 

In  the  severe  types  of  neurasthenia,  especially  when  it  occurs  in  young 
women,  the  application  of  the  "rest  cure,"  which  has  been  so  ingeniously 
elaborated  and  perfected  by  Dr.  Weir  Mitchell,  is  undoubtedly  the  best  , 
treatment.  I  do  not  find,  however,  that  men  submit  themselves  readily 
to  this  measure,  and  it  seems  to  me  to  answer  best  for  those  neurasthenic 
women  who  suffer  also  from  some  hysteria  and  who  are  reasonably  "sug- 
gestible" patients.  A  modified  rest  cure  can  often  be  secured  by  making 
the  patient  stay  in  bed  until  after  midday  lunch  or  lie  down  for  an  hour 
after  each  meal,  and  go  to  bed  early  in  the  evening.  Business  men  will 
often  cut  their  business  hours  down  one-half  if  they  are  allowed  still  to 
continue  some  work.  Experience  shows  that  in  most  cases  a  rest  is  not 
needed  for  a  very  long  period;  i.e.,  not  for  over  a  few  weeks.  Some  isola- 
tion or  change  may  be  imperative,  but  prolonged  and  absolute  rest  often 
is  not.  The  patient  is  put  to  bed  and  kept  there  for  several  days,  but  is 
soon  allowed  to  sit  up  for  a  part  of  the  day,  and  in  one  or  two  weeks  may 
begin  to  use  exercises  and  enter  upon  a  work  cure.  And  it  is  often  part 
of  the  program  to  lead  the  patient  from  abnormal  passivity  to  more  than 
ordinary  activity.  To  accomplish  this,  I  often  substitute  exercise  for 
massage,  sending  a  trainer  to  the  patient,  and  later  sending  the  patient 


528  DISEASES    OF    THE    NERVOUS    SYSTEM 

to  a  gymnasium.  Many  patients  do  best  by  putting  on  a  sweater  on 
rising  in  the  morning,  exercising  vigorously,  then  taking  a  cool  bath,  and 
then  the  breakfast.  Later  the  exercise  habit  is  inculcated,  and  this  not 
strenuously,  but  in  accordance  with  the  constitution  and  tastes  of  the 
patient. 

Exercise  is  done  to  strengthen  the  muscles,  help  the  circulation,  in- 
crease the  activity  of  the  skin,  and  keep  the  mobility  of  the  joints.  But 
it  also  should  be  of  a  kind  to  arouse  the  attention,  awaken  interest  and 
give  a  little  aesthetic  pleasure.  This  is  often  a  difficult  task,  especially 
with  women.  In  its  place  for  them  we  must  use  hot  boxes  the  masseuse, 
the  trainer — or  domestic  work. 

Horseback  riding  is  an  efficient  form  of  exercise.  Many  persons  are 
greatly  wedded  to  the  exercise  of  walking,  and  it  seems  best  to  fit  their 
needs.  It  is,  however,  a  kind  of  exercise  which  does  not  take  the  patient's 
mind  off  himself  and  does  not  develop  the  respiratory  functions  so  well  as 
other  measures  do.  Golfing  fills  in  this  lack,  and  this  sport  is  doubtless 
of  service  in  neurasthenia.  The  nurse  is  a  potent  feature  in  the  situation. 
Some  patients  are  almost  purely  exhaustion  cases,  and  only  want  rest  and 
feeding  and  sleep.  They  are  better  without  a  special  nurse.  In  other 
cases  and  oftener  a  suitable  nurse  who  is  intelligent,  tactful  and  interest- 
ing is  a  great  help. 

Change  of  scene  is  usually  very  beneficial  to  neurasthenics,  but 
traveling  is  injurious  to  them.  They  should  be  sent  to  some  special 
place  and  be  made  to  stay  there.  A  tour  along  the  Mediterranean  coast 
or  a  trip  to  Europe  often  brings  them  back  worse  than  when  they  went. 
Much  the  same  can  be  said  of  trips  to  various  places  in  the  South  or  West. 
Some  of  the  sanitaria  in  Germany,  some  of  the  places  in  the  Riviera, 
Egypt  and  Bermuda,  Nantucket,  parts  of  North  and  South  Carolina  and 
Arizona,  furnish  good  resorts  for  neurasthenics.  They  generally  do  better 
in  the  mountains,  if  the  altitude  is  not  too  high,  than  they  do  by  the  sea- 
shore. Dry,  windy,  sunny  climates  like  those  of  the  Colorado  plateau 
and  parts  of  California  and  the  Northwestern  States  are  too  stimulating 
for  most  cases. 

Much  good  may  be  obtained  at  the  numerous  sanitaria  which  exist 
in  this  country.  Many  of  these  are  well  conducted,  and  well  supplied 
with  all  the  modern  appliances  for  treatment.  It  is,  however,  always  a 
serious  thing  to  send  a  neurasthenic  to  a  sanitarium,  for  the  reason  that 
if  he  stays  there  too  long  he  becomes  contaminated  with  the  atmosphere 
of  invalidism  about  these  places  and  develops  hypochondriacal  ideas  as 
to  his  diet,  his  hver,  his  stomach,  his  sleeplessness,  and  his  various  sensory 
disturbances.  In  sending  a  patient  to  a  sanitarium  it  is  a  wise  plan  to 
tell  him  not  to  stay,  under  any  consideration,  longer  than  six  weeks; 
usually  four  is  better.     In  the  summer  time  great  benefit  can  be  secured 


NEURASTHENIA  529 

by  camping  out  in  the  woods  and  living  a  purely  outdoor  life,  away  from 
the  conventionalities  and  restraints  of  civilization. 

The  diet  of  young  neurasthenics  should  be  a  nitrogenous  one  and  my 
directions  are  that  the  patient  can  eat  meats,  fish,  eggs,  green  vegetables 
and  fruits.  Milk  can  almost  always  be  taken,  at  least  for  a  short  time. 
The  older  patients  who  do  best  upon  milk,  vegetables  and  fruit,  with 
practically  no  meat.  In  general,  tea  and  coffee,  alcohol  and  tobacco,  are 
to  be  entirely  prohibited,  but  this  is  not  an  absolute  rule.  In  some 
cases  coffee  is  beneficial,  in  some  tea  does  no  harm,  and  in  others  a  small 
amount  of  whiskey  or  dry  wine  and  a  cigar  are  also  harmless.  The 
physician  has  to  determine  this  by  the  reactions  and  habits  of  the 
patient.  Neurasthenics  usually  drink  too  little  water  and  it  is  wise  to 
prescribe  a  certain  amount  for  them.  Four  or  five  glasses  of  water, 
which  may  be  either  plain  or  alkalinized,  are  to  be  taken  daily,  unless 
the  patient  has  a  dilated  stomach  when  he  should  have  a  dry  diet.  In 
dyspeptic  patients  the  meals  should  be  small  in  amount  and  taken  at  fre- 
quent intervals;  three  light  regular  meals  a  dsLV  and  a  little  food  in 
between  form  a  regimen  which  usually  answers  well. 

Hydrotherapy,  and  massage  are  all  measures  which  prove  of  service 
to  the  neurasthenic.  Of  these,  hydrotherapy  is  the  most  useful,  though 
its  value  can  be  overestimated.  The  ordinary  prescriptions  consist  in 
the  cold  sponge  bath  every  morning,  and,  if  it  is  practicable,  the  use  of  a 
Charcot  or  a  Scottish  douche  every  other  day.  For  women  wet  packs 
with  massage  are  sometimes  helpful,  particularly  in  cases  in  which 
there  are  a  great  deal  of  nervousness  and  motor  irritation.  At  night  a 
lukewarm  bath,  at  a  temperature  of  95°,  for  ten  minutes,  sometimes 
relieves  the  sleeplessness. 

Massage  seems  to  me  of  not  very  much  use  in  men,  but  it  is  often 
grateful  and  helpful  to  women,  and  when  a  great  deal  of  rest  is  to  be 
enforced  it  is  essential  to  employ  it  for  both  sexes.  Psycho-therapy 
is  always  to  be  more  or  less  consciously  applied.  The  subject  has  al- 
ready been  discussed  and  if  I  do  not  say  more  here  it  is  because  the 
methods  of  DuBois,  suggestion,  hypnotism,  etc.,  apply  much  more 
strictly  to  the  minor  psychoses.  Neurasthenia  proper  needs  physical 
attention  to  the  body  first,  for  when  it  is  relieved  the  psychosis  may 
disappear. 

It  seemed  to  me  that  too  much  stress  is  often  laid  on  the  importance 
of  minor  troubles  of  the  pelvic  organs  in  women.  Curetting  and  sewing 
up  small  tears  rarely  do  any  good.  Serious  uterine  enlargement  and 
prolapse,  displacement  and  real  disease  of  the  ovaries  require  attention. 
If,  in  fact,  the  disorder  of  the  pelvic  organ  gives  recognized  discomfort 
it  should  be  corrected. 

Young  men  who  are  distressed  by  nocturnal  emissions  and  who  have 

34 


530  DISEASES    OF    THE    NEEVOUS    SYSTEM 

irritable  urethras  or  distended  vesicles  may  require  some  local  treatment. 
But  in  these  cases  there  commonly  is  also  a  psychosis  and  there  is  re- 
quired more  moral  than  local  therapeutics. 

The  eyes  have  received  and  need  to  receive  close  attention  for  they 
are  often  even  more  neurasthenic  than  the  stomach.  Attention  to  errors 
of  refraction  and  accommodation,  and  to  poor  muscular  balance  is  im- 
perative. Poor  eyes  may  keep  up  the  neurasthenia  and  make  the  patient 
suffer  from  the  discomforts  of  being  unable  to  read  or  to  do  close  work, 
as  well  as  give  rise  to  headaches  and  all  kinds  of  cephalic  parsesthesia. 
But  most  often  the  neurasthenia  remains  after  the  best  oculists  have  done 
all  that  is  possible.  Many  neurasthenics  continue  so  though  they  have 
good  eyes  and  can  spend  their  resting  hours  in  continuous  reading.  This 
is  my  experience  and  my  answer  to  the  insistent  claims  of  certain 
ophthalmologists  that  profound  long  continued  neurasthenia  may  be 
due  to  poorly  corrected  vision.  Such  cases  are  not  seen  by  neurologists 
now. 

The  bromide  of  sodium  or  potassium  may  be  given  to  allay  irritability 
and  insomnia;  it  should  be  kept  up  for  a  limited  time  and  then  gradually 
reduced.  At  the  same  time  or  later  the  patient  may  be  given  a  tonic 
mixture  containing  such  drugs  as  the  symptoms  suggest.  Quinine  must 
be  given  carefully,  as  it  causes  increase  of  nervousness  in  many. 

Phosphoric  and  muriatic  acids  are  the  two  mineral  acids  most  often 
of  use.  These  acids  are  usually  better  given  after  meals.  The  sac- 
charated  carbonate  of  iron  or  Blaud's  pills,  if  given,  should  be  given  gen- 
erously, i.e.,  in  doses  of  thirty  grains  daily. 

The  foregoing  covers  in  a  general  way  the  measures  to  be  used  in 
treating  neurasthenics.  It  is  really  the  treatment  of  the  neuropathic, 
and  the  constitutionally  weak,  also. 

THE  SEXUAL  NEUROSES  AND  PSYCHOSES 

Of  the  above  disorders  the  neurologist  has  to  deal  chiefly  with  the 
vicious  habits  of  masturbation  (which  may,  however,  be  also  a  mani- 
festation of  disease)  and  the  sexual  neuroses,  spermatorrhoea  and 
impotence. 

Masturbation  and  Spermatorrhoea. — Masturbation  is  the  name  given 
to  the  vicious  habit  of  artifically  exciting  the  sexual  organs.  It  is  very 
common  among  boys  and  less  common  but  present  among  girls  and  adult 
men  and  women.  It  is  usually  only  a  vice  due  originally  to  low  associa- 
tions and  teachings  among  children.  In  some  cases  it  is  a  disease  or  the 
symptom  of  a  neurotic  or  insane  constitution. 

Etiology. — It  is  most  common  between  the  ages  of  fourteen  and  eigh- 
teen, but  may  begin  earlier.     Even  infants  and  very  young  children  some- 


NEURASTHENIA  531 

times  masturbate,  usually  as  the  result  of  some  local  irritation  which 
leads  them  to  rub  the  genitals.  A  tight  prepuce,  eczema,  or  worms  may- 
lead  to  the  habit,  but  is  it  usually  taught  by  a  companion.  The  practice 
sometimes  attacks  schools  almost  hke  an  epidemic,  for  in  every  institu- 
tion a  certain  per  cent,  of  the  boys  are  sexually  precocious  or  vicious, 
while  the  others  are  ignorant  and  innocent  of  the  evils  of  the  practice. 
Masturbation  is  relatively  rare  after  twenty,  but  is  practised  by  some 
throughout  life  even  up  to  old  age. 

Symptoms.— Masturbation,  as  ordinarily  practised,  leads  after  a 
time  to  a  feeling  of  malaise,  mental  depression,  disinclination  to  work, 
study,  or  to  enjoy  one's  self  as  before.  The  appetite  is  a  little  impaired, 
the  extremities  easily  get  cold  and  perspire  readily.  Pecuhar  numb 
feelings  are  felt  in  the  hands  and  feet.  There  are  an  unnatural  nervous- 
ness and  irritability,  and  the  power  of  concentrating  the  mind  is  a  little 
weakened.  The  patients  often  have  dilated  pupils  and  hypersesthetic 
skin.  After  a  time  nocturnal  emissions  occur.  The  organs  become  ir- 
ritable and  slight  excitement  causes  erections.  These  symptoms  may  be 
slightly  marked  and  pass  away  in  a  day  or  two,  or  until  another  indul- 
gence occurs. 

Masturbation  is  sometimes  done  to  an  extraordinary  extent,  even 
daily  or  twice  daily  for  a  considerable  time.  After  a  while  the  young 
man  begins  to  find  that  he  is  not  well  and  realizes  that  his  habit  is  hurting 
him.  Then  if  he  be  sensible  and  of  healthy  constitution  he  stops.  Others 
are  frightened  out  of  it  by  friends  or  by  reading  the  terrorizing  stories 
printed  in  quack  advertisements  and  circulars.  Sometimes  the  fright 
thus  caused  leads  the  unhappy  youth  into  a  condition  of  hypochondriasis, 
which  is  helped  on  by  the  occurrence  of  nocturnal  pollutions  and  the  ner- 
vous debility  resulting  from  his  past  indiscretions.  In  other  cases  in 
which  there  is  a  decided  neurotic  history,  a  genuine  neurasthenia  of  a 
sexual  type  develops  and  annoys  the  patient  for  years. 

Masturbation  rarely  leads  to  insanity  and  is  oftener  a  symptom  than 
a  cause  of  such  disorder.  It  is  perhaps  most  often  associated  with  de- 
mentia prsecox.  It  is  occasionally  the  cause  of  epilepsy.  When  this  is 
the  case  the  convulsive  attacks  are  likely  to  put  on  a  hysteroid  phase  and 
are  accompanied  by  peculiar  co-ordinated  convulsions  and  emotional 
disturbance.  Masturbation  is  the  common  cause  of  hystero-epilepsy  in 
women. 

Diagnosis. — Many  victims  of  the  masturbation  habit,  who  have  come 
to  recognize  its  evils  and  tried  to  stop  it,  develop  a  hypochondriacal  con- 
dition, and  feel  sure  that  there  is  something  in  their  faces  which  reveals 
to  the  world  their  trouble.  This  is  not  the  case.  But  there  is  a  certain 
physiognomy  which  in  a  measure  characterizes  the  masturbator  to  such 
an  extent  that  an  experienced  observer  can  detect  it.     The  pale,  pasty 


532  DISEASES    OF   THE    NERVOUS    SYSTEM 

complexion,  moist,  furtive  eye,  dilated  pupil,  listless,  restless,  and  de- 
pressed manner,  the  wet,  flabby  palms,  and  hypersesthetic  skin,  all  help 
to  tell  the  story.  Locally,  the  penis  is  often  reddened  and  more  or  less 
turgid,  the  scrotum  relaxed,  and  a  varicocele  may  be  present.  Examina- 
tion of  the  urine  may  reveal  spermatozoa.  The  urine  also  is  almost 
always  of  rather  low  specific  gravity,  and  contains  a  great  excess  of  phos- 
phates, both  earthy  and  alkaline. 

Treatment. — The  patient  must  be  told  plainly  the  necessity  of  stop- 
ping the  practice.  He  must  be  impressed,  but  not  terrorized.  He 
should  be  kept  out  of  doors  at  vigorous  physical  exercise,  for  sedentary 
and  solitary  work  is  always  bad  for  such  cases.  He  should  be  made  to 
take  cold-water  baths  and  should  sleep  on  a  hard  bed  with  light  covering. 
He  had  better  sleep  with  some  one  whose  presence  may  exercise  a  con- 
trolling influence.  He  should  not  eat  heartily  at  night,  never  just  before 
going  to  bed.  And  what  is  still  more  important,  he  should  not  drink 
before  going  to  bed.  Sometimes  it  is  well  to  have  him  wakened  at  an 
early  hour  in  the  morning,  when  he  should  empty  his  bladder;  for  emis- 
sions occur  often  early  in  the  morning  and  are  promoted  by  the  irritation 
of  a  full  bladder. 

Locally,  cold-steel  sounds  may  be  introduced  and  allowed  to  remain 
for  ten  minutes,  three  or  more  times  a  week,  or  the  psychophor  or  Ultz- 
mann's  short  catheter  may  be  used.  In  bad  cases  with  a  great  deal  of 
prostatic  irritation,  local  applications  of  nitrate  of  silver  are  needed. 
Internally,  a  mixture  of  tinct.  opii,  tinct.  camph.,  and  tinct,  lupulin  may 
be  given  at  night,  the  ingredients  being  somewhat  varied  in  amount  to 
suit  the  case.  Bromides,  chloral,  atropine,  and  salix  nigra  are  also  drugs 
which  are  often  useful.  The  mechanical  measures  which  have  been  de- 
vised for  preventing  erections,  such  as  rings  with  sharp  teeth,  are  rarely 
needed  and  rarely  useful.  They  may  even  do  harm  by  directing  the  mind 
to  the  affected  function. 

I  do  not  believe  it  right  for  the  physician  to  prescribe  fornication. 
It  is  not  safe  nor  curative,  apart  from  the  moral  aspect  of  the  matter.  It 
has  always  struck  me  also  as  pretty  small  business  for  a  man  purposely 
to  select  a  wife  to  relieve  him  of  the  results  of  a  weak  will  and  vicious  sen- 
sual indulgence.  If  marriage  comes  in  the  natural  course  of  events,  as 
it  often  does,  so  much  the  better.  But  to  select  a  wife  as  a  remedial  agent 
for  masturbation  is  unjust  to  the  woman  and  a  confession  of  moral  and 
mental  feebleness.  Man  is  distinguished  from  the  brute  by  his  self- 
control.  Let  him  bear  this  fact  in  mind  and  raise  himself  above  the  ani- 
mals by  a  determined  effort  of  the  will.  Pure  thoughts  and  chaste  as- 
sociations, vigorous  physical  exercise,  and  a  resolute  effort  to  act  a  manly 
part  will  always  be  successful. 


NEURASTHENIA  533 

TRAUMATIC  NERVOUS  AFFECTIONS 

{Traumatic  Neuroses  and  Psychoses,  Spinal  Concussion) 

The  present  tendency  of  neurology  is  to  deny  the  existence  of  any 
special  nervous  affection  produced  by  trauma  or  shock.  There  may  fol- 
low from  these  causes: 

1.  Surgical  injuries. 

2.  Neurasthenic  and  morbid  psychic  states. 

3.  Hysterical  states. 

4.  Hemorrhagic,  inflammatory,  and  degenerative  diseases. 

5.  Combinations  of  the  foregoing. 

These  troubles  may  follow  not  only  railway  but  other  injuries,  but  are 
especially  liable  to  follow  those  associated  with  intense  fright. 

2.  Traumatic  neurasthenia  or  "traumatic  neurosis,"  '"railway  spine," 
does  not  differ  from  forms  of  neurasthenia  produced  by  other  causes,  ex- 
cept that  with  it  there  may  be  certain  sprains  and  surgical  troubles  and 
some  morbid  mental  condition.  Its  special  symptoms  are  described 
under  the  head  of  neurasthenia. 

3.  Traumatic  hysteria  is  a  rare  affection  in  this  country.  It  does  not 
differ  from  hysteria  produced  by  other  causes,  except  for  its  sudden  onset 
and  occasional  surgical  complications.  It  is  usually  a  hysteria  major 
and  has  the  characteristic  stigmata  of  that  type.  In  this  city  electrical 
injuries  and  frights  have  produced  some  classical  cases  of  hysteria  major. 

4.  There  is  considerable  evidence  that  in  some  rare  cases  traumatism 
may  produce  minute  multiple  hemorrhages  throughout  the  nervous 
centres.  In  such  cases  there  are  usually  neurasthenic  or  hysterical 
symptoms  and  in  addition  symptoms  of  organic  disease. 

Massive  hemorrhages  and  serious  mechanical  injury  of  the  nervous 
centres  may  be  also  produced  by  injury. 

Finally,  it  is  a  well-known  fact  that  traumatisms  may  excite,  in  the 
predisposed  and  the  infected,  locomotor  ataxia  inebriety,  insanity  or 
may  lead  to  the  development  of  a  cerebral  tumor. 

It  is  the  mental  impression,  the  shock,  much  more  than  the  physical 
injury,  which  produces  the  functional  neurosis  or  psychosis. 

The  symptoms  may  appear  soon  after  the  accident,  or,  after  a  period 
of  relative  health  lasting  some  weeks  the  neurosis  gradually  develops. 
The  most  important  practical  point  in  connection  with  the  subject  is 
the  diagnosis  and  the  elimination  of  malingering.  This  is  additionally 
difficult  for  the  reason  that  the  hopes  and  anxieties  depending  upon  litiga- 
tion tend  to  cause  introspection,  exaggeration  of  symptoms  and  uncon- 
scious bias  even  in  the  most  honest.  The  opinion  among  American 
neurologists  tends  to  favor  the  reality  of  traumatic  neuroses.  "While 
malingering  is  not  rare,  yet  if  the  patient  has  really  a  traumatic  neuras 


534  DISEASES    OF    THE    NERVOUS    SYSTEM 

thenia  or  hysteria  the  disease  may  not  be  a  trifling  one.  Careful  research, 
however,  often  tends  to  eHcit  the  fact  that  previous  to  the  injury  the  pa- 
tient was  an  alcohoHc,  syphihtic,  or  neurotic,  and  perhaps  had  already 
the  beginning  of  his  alleged  traumatic  disorder.  In  no  part  of  clinical 
medicine  is  a  careful  and  searching  examination  and  weighing  of  symp- 
toms more  urgently  called  for.  The  methods  of  carrying  out  such  ex- 
aminations are  given  elsewhere.  Special  methods  for  testing  anaesthesia 
are  sometimes  needed.  The  two  sides  of  the  body  should  be  tested  simul- 
taneously with  concealed  needles,  beginning  on  the  trunk,  or  the  faradic 
current  with  a  double-pointed  electrode  maj^  be  used.  There  are  few 
patients  who  can  successfully  deceive  in  an  examination  covering  all  the 
special  senses. 

The  treatment  of  these  neuroses  calls  for  no  special  notice  here. 


CHAPTER  XXIV 
THE  MYOCLONIAS  OR  TWITCHING  SPASMS 

(Chorea — The  Spasmodic  Tics) 

Myoclonia  is,  or  should  be,  a  general  term  used  for  twitching  spasms 
of  all  kinds.  Strictly  speaking,  it  includes  chorea,  the  convulsive  tics, 
paramyoclonus  multiplex,  certain  hysterical  spasms,  myoclonus  epilepsy; 
also  myokimia  or  fibrillary  and  wave-like  twitchings,  and  rhythmic 
myoclonia. 

Myotonia,  or  tonic  spasm,  is  a  general  term  used  to  designate  tonic 
spasms  such  as  those  of  tetanus,  tetany,  the  symptomatic  tonic  spasms 
of  organic  disease  and  hysteria,  myotonia  congenita  or  Thomson's  disease 
and  myotonia  acquisita. 

Myoclonus  is  a  special  term  indicating  the  twitching  of  a  muscle. 

Myotonus  indicates  the  tonic  contraction  of  a  muscle.  The  patient 
has  a  myoclonia;  the  muscle  is  in  myoclonus.  The  term  myoclonia  has 
been  much  misused,  and  there  is  great  confusion  in  the  nomenclature. 

There  are  five  more  or  less  distinct  clinical  types,  but  these  can  be 
with  sufficient  accuracy  reduced  to  three: 

1.  Infectious  myoclonia,  which  is  the  chorea  of  Sydenham. 

2.  Psychogenic  and  degenerative  myoclonias  which  include  the  spas- 
modic tics,  and  hereditary  chorea. 

3.  The  myokimia  disorders,  which  include  various  symptomatic 
fibrillary  and  wave-like  twitchings,  and  the  so-called  myoclonus  multiplex 
of  Friedreich. 

The  twitching  and  tonic  spasms  and  gross  tremor  often  occur  in  the 
same  disorder  and  we  need  terms  like  myoclonus-tonus  and  myoclono- 
tonia  to  indicate  these  combinations. 

CHOREA  OF  SYDENHAM 

{St.  Vitus^s  Dance) 

This  is  the  common  type  of  chorea,  and  is  the  disease  ordinarily  meant 
when  the  term  chorea  is  used.  It  is  a  subacute  disorder  characterized 
by  irregular,  inco-ordinate  twitching  movements.  The  disease  is  a 
common  one,  forming  about  one-fifth  of  the  nervous  diseases  of  children. 

Etiology. — Most  cases  occur  between  the  ages  of  five  and  fifteen. 
It  is  very  rare  under  five.     A  few  cases  occur  after  twenty,  and  even  up 

535 


536  DISEASES    OF    THE    NERVOUS    SYSTEM 

to  old  age,  when  a  senile  chorea  is  sometimes  observed.  It  affects  girls 
more  than  boys  in  the  ratio  of  about  2.5  to  1.  In  adult  life  the  dispro- 
portion is  less  marked.  It  is  relatively  rare  in  the  negro  race,  especially 
in  those  of  pure  blood  (Mitchell).  It  occurs  in  all  climates.  Most  cases 
develop  in  the  spring  months,  next  in  the  autumn,  next  in  winter,  and 
last  in  summer.  The  seasonal  influence  varies  in  different  localities. 
School  attendance  and  work  have  something  to  do  with  these  variations. 
The  disease  is  more  frequent  in  cities,  and  in  the  poorer  classes. 
Hereditary  influence  is  slight,  but  it  exists.  In  a  small  percentage  of 
cases  one  parent  has  had  chorea,  epilepsy,  insanity,  or  a  decided 
neuropathic  constitution. 

The  chief  exciting  causes  are  injury  and  fright,  mental  worry,  and 
some  infection,  generally  a  rheumatic  or  tonsillar  one.  Fright  or  some 
emotional  disturbance  is  a  cause  in  about  one-fifth  of  the  cases.  Acute 
rheumatism  is  given  as  a  cause  in  very  varying  proportions,  ranging  from 
15  to  20  per  cent.  Some  authors  lay  much  stress  on  rheumatism 
and,  counting  attacks  of  tonsillitis  as  evidence  of  rheurnatism,  they  find 
it  a  large  causal  factor.  Endocarditis  is  developed  in  the  course  of  chorea 
in  about  one-fourth  of  the  cases,  and  this  may  exist  without  any  other 
manifestations  of  rheumatism.  Pregnancy  is  a  cause  of  chorea,  generally 
in  primiparse  and  in  young  women  under  twenty-five.  Chorea  sometimes 
follows  infectious  fevers,  especially  measles,  scarlatina  and  whooping- 
cough.  Chorea  is  the  prominent  symptom  in  some  septic  cases,  of  which 
septic  chorea  (Sachs),  and  the  serious  mental  disorder  known  as  chorea 
insaniens  are  examples.  Overstudy  and  the  worry  of  examinations  are 
factors  in  causing  chorea  in  predisposed  and  badly  nourished  children; 
and  anaemia  and  malnutrition  underlie  most  cases. 

Symptoms.- — The  disease  may  begin  suddenly,  but  usually  it  develops 
slowly,  and  it  is  not  till  one  or  two  weeks  that  the  symptoms  are  decidedly 
prominent.  It  usually  begins  with  irregular  twitching  of  the  hand  or 
face  on  one  side.  The  child  winks,  grimaces,  jerks  its  head  or  shoulder, 
twitches  its  arms  and  drops  things  from  its  hand.  The  foot  and  leg 
become  affected  later  and  the  child  stumbles  in  walking.  In  two  or  three 
weeks  the  opposite  side  is  involved,  but  usually  less  than  the  one  originally 
affected.  In  three  or  four  weeks  the  disease  reaches  its  height.  The 
patient's  movements  are  then  almost  continuous.  The  hands  can  hardly 
be  used  and  the  child  has  to  be  fed  and  dressed;  even  walking  is  awkward 
and  difficult.  Speech  is  indistinct  and  confused  from  the  irregular  move- 
ments of  the  lips  and  tongue.  An  actual  mutism  may  occur.  The  mus- 
cles of  respiration  may  be  involved  so  that  the  rhythm  is  uneven. 

The  choreic  movements  usually  occur  both  when  the  muscles  are  at 
rest  and  during  volitional  acts.  In  some  cases  the  disease  is  chiefly 
characterized   by  inco-ordinate  movements  when  purposeful  acts   are 


THE    MYOCLONIAS    OR   TWITCHING    SPASMS 


537 


attempted.  In  other  eases  voluntary  movements  can  be  readily  per- 
formed, and  the  muscles  twitch  only  when  the  limbs  are  at  rest.  The 
movements  cease,  as  a  rule,  during  sleep.  But  the  child  sometimes 
gets  to  sleep  with  difficulty  on  account  of  the  movements.  In  severe 
cases  attacks  of  mental  excitement  and  even  delirium  come  on  for  several 
successive  nights.  Apart  from  such  incidents,  the  mind  in  chorea  is 
usually  dulled,  the  temper  irritable,  and  the  child  much  harder  to 
manage  (Fig.  233). 

The  appetite  is  poor  and  capricious,  the  tongue  coated,  and  the  bowels 
are  often  constipated.     The  nutrition  fails  a  little;  there  are  anaemia  and 


Fig.  233. — Chorea,  showing  grimace  and  shoulder  movement.     (Jacobsohn.) 


a  tendency  to  loss  of  flesh.  The  eyes  present  nothing  abnormal. 
Hypermetropia,  astigmatism,  and  muscular  insufficiencies  exist,  but  not 
much  more  than  in  other  nervous  children. 

The  child  is  often  worse  in  the  morning  and  improves  toward  night. 
Excitement  and  physical  exertion  make  the  movements  worse.  There  is 
rarely  any  pain  and  never  ansesthesia  or  tenderness.  The  muscles  are 
weak  but  not  actually  paralyzed.  The  deep  reflexes  are  somewhat 
lessened  and  the  knee-jerk  may  be  abolished.  In  a  good  many  cases 
the  so-called  "tonic  reflex"  is  present.  When  the  patella  tendon  is 
struck  the  foot  flies  up,  and  instead  of  dropping  back  at  once  remains  up 
for  a  second  or  more;  or  a  second  slight  reinforcing  jerk  occurs.     The 


538  DISEASES    OF    THE    NERVOUS    SYSTEM 

electrical  irritability  of  the  muscles  is,  as  a  rule,  increased,  but  there  are 
no  qualitative  changes.  Nocturnal  enuresis  occasionally  occurs.  The 
urine  contains  an  excess  of  urea  and  phosphates  and  at  the  height  of  the 
attack  the  specific  gravity  may  be  increased. 

Forms. — -Maniacal  chorea  or  chorea  insaniens,  is  characterized  by  fever, 
choreic  movements  and  great  mental  excitement — especially  at  night, 
with  delirium,  hallucinations  and  delusions.  The  patient  has  in  effect 
a  toxic  or  infectious  psychosis.  After  two  or  three  weeks  the  excitement 
lessens  and  the  patient  becomes  dull  and  apathetic.  Such  cases  usually 
occur  in  adult  women,  and  they  are  often  fatal. 

Paralytic  chorea.  In  this  form  one  arm  or  one  side  of  the  body  be- 
comes rather  weak  and  powerless.  A  few  twitching  movements  are  ob- 
served. This  form  occurs  only  in  children  and  runs  the  same  course  as 
the  spasmodic  type. 

Chorea  of  adult  life  and  senile  chorea.  The  disease  when  it  occurs 
in  the  second  half  of  life  attacks  men  rather  oftener  than  women;  it  is 
of  toxic  or  infectious  origin,  but  not  related  to  rheumatism.  There  is 
usually  a  neurotic  family  history  of  chorea.  The  attack  is  usually  excited 
by  emotional  disturbances.  It  runs  much  the  same  course  as  juvenile 
chorea,  but  is  rather  more  apt  to  become  chronic.  When  it  occurs  in 
old  men  it  is  called  senile  chorea.  This  type  is  not  to  be  confounded  with 
hereditary  or  Huntington's  chorea. 

Duration — Relapses. — ^The  disease  in  this  country  lasts  about  ten  or 
twelve  weeks,  ranging,  however,  from  six  weeks  to  six  months.  There 
may  be  great  improvement  followed  by  a  relapse,  and  in  this  remittent 
manner  the  disease  may  last  for  years.  If  it  lasts  more  than  six  months 
it  should  be  called  chronic.  Relapses  occur  in  about  one-third  of  the  cases 
and  rather  oftener  in  girls.  Relapses  occur  oftenest  within  a  year  of 
the  first  attack  and  much  oftener  in  the  spring.  After  three  years  re- 
lapses practically  cease.  The  number  of  relapses  is  usually  but  one, 
but  the  disease  may  recur  eight  or  nine  times.  Relapses  rarely  occur  in 
adults  except  in  the  chorea  of  pregnancy. 

Pathology. — Chorea  has  no  definite  anatomical  basis,  though  the  seat 
of  the  disease  is  in  the  brain.  The  irritant  seems  to  come  from  and  act 
first  upon  the  blood-vessels,  causing  in  severe  cases  intense  hypersemia, 
with  dilatation  of  vessels,  small  hemorrhages,  and  spots  of  softening. 
There  are  infiltration  of  the  perivascular  spaces  with  round  cells  and  swell- 
ing and  proliferation  of  the  intima  of  the  small  arteries.  In  chronic  cases 
the  evidence  of  active  vascular  irritation  is  less,  but  there  are  perivascular 
dilatations  and  increase  of  connective  tissue.  The  process  suggests  a  low 
grade  or  an  initial  stage  of  inflammation.  The  cause  of  this  is  usually 
an  infective  micro-organism  similar  to  that  causing  the  rheumatic  symp- 


THE    MYOCLONIAS    OR   TWITCHING    SPASMS  539 

toms  and  the  heart  lesions.  The  infection,  is  sometimes  and  perhaps 
commonly  due  to  the  micrococcus  viridans.  In  a  considerable  per  cent, 
of  cases  (90  per  cent. — Osier)  especially  in  those  of  long  duration, 
there  are  fibrinous  deposits  on  the  walls  of  the  heart.  The  presence 
of  points  of  irritation  in  the  cortex  and  its  meninges  and  in  the 
deeper  parts  excites  irregular  discharges  of  nerve  force  and  produces 
the  choreic  movements.  The  interruption  of  the  voluntary  nerve  im- 
pulses by  diseased  foci  makes  these  movements  irregular.  In  para- 
lytic chorea  the  pyramidal  tract  is  probably  more  seriously  injured 
by  some  single  large  focus  of  congestion,  exudation,  or  hemorrhage. 
Indeed,  I  have  seen  a  true  hemiplegia  develop  in  the  midst  of  an  attack. 
In  maniacal  chorea  the  meninges  and  cortex  are  more  involved. 

Diagnosis. — The  disease  is  easily  recognized  by  the  peculiar  twitching 
movements.  It  must  be  distinguished  from  convulsive  tic,  hereditary 
chorea,  hysterical  spasms  which  include  saltatorj^  chorea  and  chorea 
major.  The  distinctions  are  not  difficult  and  are  given  in  connection 
with  the  descriptions  of  these  disorders. 

Prognosis. — As  regards  life,  the  prognosis  is  very  favorable.  In  this 
country  death  from  chorea  hardly  ever  occurs  in  children.  It  is  more 
fatal  in  adults,  and  especially  in  pregnant  women.  This  is  the  statement 
of  European  writers.  I  have  never  seen  a  mortality  and  many  cases  of 
chorea  of  pregnancy  have  been  observed  in  my  service  at  Bellevue  Hos- 
pital.    Nearly  all  non-fatal  cases  eventually  get  well  of  the  chorea. 

Treatment. — The  most  important  single  factor  in  treatment  is  rest. 
The  child  should  not  be  allowed  to  take  violent  exercise  or  to  have  any 
excitement.  In  most  cases  he  should  be  taken  from  school,  and  in  bad 
cases  he  should  be  kept  in  bed.  In  all  cases  he  should  be  largely  isolated 
and  kept  quiet.  Cold  packs  should  be  given  once  or  twice  daily,  if  the 
movements  are  violent.  Cold  sponging  or  douching  daily  along  the  back 
is  often  sufficient. 

As  specific  remedies,  arsenic  should  be  given  in  doses  of  TTLv.  of  Fowler's 
solution  t.i.cl.,  increased  by  one  or  two  drops  daily  to  fifteen  or  twenty 
drops  or  even  more.  If  this  causes  nausea  and  gastric  pain  or  headache, 
the  dose  should  be  stopped  for  a  day  and  then  resumed,  if  possible,  where 
it  was  left  off.  The  bromide  of  zinc  is  also  an  excellent  remedy,  when 
there  is  a  hysterical  element.  CHoral  is  most  useful  in  violent  cases 
especially  when  the  patient  can  not  sleep. 

Hyoscine  hydrobromate  in  doses  of  gr.  3^f  oo  is  occasionally  efficacious. 
The  salicylates  are  now  much  used  in  the  acute  hospital  cases.  In  chronic 
and  obstinate  cases  hypodermic  injections  of  the  cacodylate  of  soda  may 
be  tried.  A  most  potent  remedy  in  some  severe  acute  cases  is  the  injec- 
tion of  neo-salvarsan. 


540  DISEASES    OF    THE    NERVOUS    SYSTEM 

HEREDITARY  CHOREA 

{Huntington'' s  Chorea) 

Hereditary  chorea  was  first  described  by  a  Long  Island  physician, 
Dr.  Waters,  in  1842,  later  by  Drs.  Gorman  and  Lyon,  and  in  ■  1872 
by  Dr.  Huntington  to  whom  most  credit  for  establishing  the  symptoms 
is  due.  The  American  cases  have  been  observed  chiefly  in  New  York, 
Connecticut,  New  Jersey,  and  Pennsylvania.  Cases  have  been  re- 
ported also  from  Germany,  France  and  England.  The  disease  begins 
before  thirty  and  not  after  fifty;  it  occurs  about  equally  in  males  and 
females.  It  is  almost  always  directly  hereditary,  either  through  father 
or  mother,  usually  the  latter.  It  begins  without  known  cause  by  twitch- 
ings  in  the  face;  the  movements  then  extend  to  the  arms  and  legs.  The 
movements  are  very  much  like  those  of  chorea  minor.  They  are,  how- 
ever, apt  to  become  more  jerky  and  violent;  the  legs  are  especially  sub- 
ject to  jerky  movements,  causing  difficulty  and  grotesqueness  of  gait. 
A  patient  of  mine  used  to  be  frequentlj^  thrown  out  of  bed  by  the  move- 
ments. They  can,  however,  often  be  voluntarily  controlled  for  a  time. 
The  speech  is  early  affected.  There  is  no  paralysis  or  disturbance  of 
sensibility.  The  disease  is  attended  by  progressive  mental  deterioration, 
sometimes  by  a  tendency  to  melancholia,  and  usually  ends  in  dementia. 
Its  course  is  chronic  and  very  slow,  lasting  ten  or  twenty  years.  Post- 
mortem, chronic  pachymeningitis  and  leptomeningitis  with  degenerative 
changes  in  the  cells  of  the  motor  cortex  have  been  found. 

Electric  Chokea  is  a  name  sometimes  and  wrongly  given  to  very  violent  forms  of 
the  ordinary  chorea  of  Sydenham.  The  term  was  first  applied  by  Dubini  to  a  peculiar 
and  progressively  fatal  spasmodic  affection  which  has  been  observed  almost  solely  in 
Italy,  and  which  is  perhaps  of  a  podagrous  or  malignant  malarial  origin.  M.  Bergeron 
in  1880  also  described  an  "electric  chorea"  in  which  the  patients  are  attacked  by  sudden 
rhythmical  spasms.  This  latter  disease  has  a  uniformly  favorable  course.  Neither 
of  these  diseases  resembles  true  chorea,  nor  do  they  have  the  character  of  the  tics. 

The  term  electric  chorea,  therefore,  is  one  that  should  be  used,  if  at  all,  only  with  a 
qualifying  explanation. 

PROcuRsrvE  Chorea,  or  Dancing  Chorea. — Laycock  has  described  as  a  separate 
kind  of  chorea  a  rhythmical  or  trochaic  form,  which  he  says  affects  children,  principally 
girls,  and  shows  itself  in  spasmodic  rhythmical  contractions  or  in  sudden  rotating  or 
procursive  movements  of  the  body.  This  has  been  called  chorea  procursive,  or  chorea 
festinans,  by  other  writers.  In  many  cases  it  is  accompanied  by  vertigo,  when  the 
condition  of  the  patient  is  similar  to  that  of  a  person  who  has  been  whirling  around  a 
number  of  times.  Such  cases  always  have  decidedly  hysterical  characters,  although 
these  procursive  attacks  may  complicate  ordinary  chorea. 

Chorea  Major  is  a  manifestation  of  hysteria,  and  has  been  described  under  that 
head.     It  is  not  a  chorea  at  all. 


THE    MYOCLONIAS    OR    TWITCHING    SPASMS  541 

SPASMODIC   TIC 

{Mental  Tics,  Habit  Tics,  Hysterical  Tics,  Local,  General  and  Endemic  Tics) 

Spasmodic  tic  is  a  disease  to  which  the  name  of  chorea  is  often,  but 
incorrectly  given.  It  is  a  very  chronic  disorder,  and  shows  itself  in  the 
form  of  quick,  electric-like  spasms  of  certain  groups  of  muscles  or  single 
muscles.  With  this  there  occur  short  tonic  and  rhythmical  movements. 
The  twitching  movements  differ  from  those  of  chorea  in  that  groups  of 
muscles  physiologically  related  are  affected  and  co-ordinated  movements 
result. 

1.  There  are  local,  habit  and  psychic  tics. 

2.  Generalized  tics  with  tonic  and  rhythmical  movements. 

3.  Tics  associated  with  other  diseases,  e.g.,  myoclonus  epilepsy. 

4.  Hysterical  tics. 

1.  Habit,  Local  and  Psychic  Tics. — There  are  many  persons  who  go 
through  life  with  some  trick  of  speech,  of  gesture,  or  some  peculiar  grim- 
ace. It  may  be  only  a  shrug  of  the  shoulder,  a  twitching  of  the  eyes, 
or  a  sniff.  These  various  movements  are  tics  of  the  co-ordinate  kind. 
The  spasmodic  motion  is  of  itself  normal,  but  is  inappropriate  and 
misapplied. 

Such  movements  are  often  seen  in  children.  They  sometimes  rep- 
resent abortive  attacks  of  chorea,  and  sometimes  they  are  the  residuum 
of  old  attacks.  In  these  tics,  a  reflex  or  central  irritation  often  sets  up 
the  spasm.  This  irritation,  such,  for  example,  as  that  of  an  eye-strain 
or  a  nasal  disorder  is  removed,  and  subsides  from  consciousness;  but 
the  subconscious  feeling  of  it  remains  and  produces  a  response,  such  as 
the  grimace  or  the  sniffling. 

Closely  allied  to  habit  tics  are  various  local  tics.  Thus  when  the 
spasm  is  localized  in  the  facial  nerve,  we  have  a  facial  or  mimic  tic  (see 
p.  105).  The  spasm  may  become  localized  even  in  a  single  branch  of  a 
nerve,  as  that  to  the  orbicularis,  the  zygomaticus,  the  diaphragm,  or  the 
tensor  tympani.  Spasmodic  tic  sometimes  involves  the  trunk  and  legs. 
It  may  attack  the  muscles  of  expiration  and  the  larynx,  and  then  it  has 
been  called  chorea  of  the  larynx. 

Spasmodic  tics  are  sometimes  accompanied  by  explosive  disturbances 
of  speech.  In  these  cases  the  patient  at  the  time  of  the  convulsive  move- 
ment utters  some  obscene  or  profane  words  (coprolalia) ,  or  involuntarily 
repeats  the  last  words  of  the  sentence  spoken  to  him  (echolalia) ,  or  spas- 
modically imitates  a  gesture  made  to  him  (echokinesis) ,  or  involuntarily 
exclaims  the  thought  uppermost  in  his  mind,  perhaps  revealing  some 
secret  against  his  will  (tic  de  pensee).  These  speech-tics  may  occur  with- 
out any  other  motor  manifestation,  and  a  tendency  to  exclamatory  tics 
is  not  uncommon  in  ordinary  life. 


542  DISEASES    OF    THE    NERVOUS    SYSTEM 

2.  Generalized  Tics  {Degenerative  Tics). — The  convulsive  movements 
here  take  a  wide  range  and  affect  a  number  of  groups  of  muscles,  produc- 
ing quick,  violent  movements  of  the  face,  head,  extremities  and  trunk, 
associated  with  short  tonic  spasm  of  the  affected  parts. 

Generalized  tics  affect  children  from  birth  or  develop  between  the 
ages  of  six  and  sixteen  years,  and  by  preference  the  masculine  sex.  There 
is  almost  always  a  neurotic  and  sometimes  a  hereditary  family  history. 
The  children  are  nervous,  excitable,  often  retarded. 

The  disease  begins  with  attacks  of  spasmodic  movements,  affecting 
generally  the  head,  face  and  upper  extremities  first,  then  perhaps  involv- 
ing the  whole  body.  The  movements  can  be  controlled  for  a  time  by 
the  will,  only  to  break  out  with  increased  violence  later.  They  cease 
during  sleep,  which  is  generally  profound. 

Degenerative  generalized  tics  are  chronic  and  incurable. 

When  there  is  no  gross  change  the  brain  shows  an  irregular  arrange- 
ment and  defective  number  of  the  cells  of  the  motor  cortex.  Sometimes 
the  brain  is  found  damaged  by  infection,  or  an  early  cerebral  diplegia. 

The  treatment  of  tics  is  dealt  with  in  connection  with  certain  special 
types,  e.g.,  facial  tic,  torticollis,  writer's  cramp.  It  is  essentially  hygienic 
and  pedagogic.  In  the  mild  forms  of  habit  spasm  of  children,  bromide 
of  zinc  in  doses  of  gr.  ii.  to  tolerance  is  a  very  efficient  drug. 

Spasmodic  tic  may  be  associated  with  epilepsy  (myoclonus  epilepsy). 
Of  this  there  is  a  special  familial  type  (Unverricht). 

Hysterical  or  psychogenous  tics  may  simulate  the  local  and  the  degen- 
erative forms.  They  are  not  so  severe  or  general  in  their  manifestations 
and  are  more  apt  to  be  manifestations  of  a  sexual  complex,  the  results  of 
mimicry  and  a  psychological  contagion  like  the  dancing  manias  of  former 
centuries. 

The  peculiar  disorder  of  the  Maine  ''jumpers,"  characterized  by  sud- 
den violent  movements  on  being  touched  or  startled,  is  a  form  of  endemic 
hysterical  tic.  The  chseases  known  as  latah,  occurring  in  Malay,  and 
myriachit,  occurring  in  Siberia  and  Kamchatka,  are  also  endemic  and 
probably  hysterical  tics. 

FIBRILLARY  MYOCLONIA 

(Myoclonus  Multiplex  of  Friedreich)  ' 

The  exact  nature  of  this  rare  disease  has  been  misunderstood.  It  is 
probably  due  to  some  infection,  but  in  the  original  case  it  followed  a 
fright.  It  occurs  mostly  in  adult  males.  In  the  description  of  the  disease 
one  cannot  improve  on  that  originally  given  by  Friedreich.  He  states 
that  it  is  a  peculiar  affection  of  the  muscles,  especially  of  the  upper  and 
lower  extremities,  showing  itself  in  the  form  of  short  rapid  contractions, 
reappearing  at  short  intervals,  which  affect  individual  muscles  of  the 
arms  and  forearms,  thighs,  trunk  and  face. 


THE    MYOCLONIAS    OE    TWITCHING    SPASMS  543 

It  is  not  merely  fibrillary  or  fascicular  twitchings,  but  a  spasm  which 
involves  the  whole  of  the  muscle  which  swells  in  a  mass,  and  bulges  every 
time,  even  when  the  contractions  of  the  muscles  were  not  marked  enough 
to  produce  a  noticeable  motor  effect  on  the  limbs  to  be  moved.  Only 
at  times,  at  an  unusually  marked  contraction,  one  notices  a  slight  change 
in  the  part  to  be  moved,  e.g.,  during  many  contractions  of  the  biceps  a 
slight  flexion  of  the  forearm  or  during  some  of  the  spasms  of  the  supinator 
longus  a  slight  supination  of  the  hand. 

The  spasms,  are  unrhythmical  throughout  and  varying  in  extent, 
even  though  they  are  separated  from  each  other  only  by  short  intervals. 
By  placing  the  stethoscope  on  the  affected  muscles  in  themoment  of  their 
contraction,  a  loud  and  clear  sound,  resembling  the  first  heart  sound  in 
every  respect,  can  be  appreciated. 

Every  muscle  shows  a  complete  independence  in  relation  to  its  indi- 
vidual contractions.  Now  it  was  this  muscle,  now  that  muscle,  which 
twitches  all  for  itself  without  any  relation  to  the  others,  and  if  it  some- 
times happens  that  the  contraction  of  a  muscle  on  one  side  takes  place 
synchronously  with  another  muscle  of  the  same  or  other  side,  or  even  at 
times  if  two  symmetrical  muscles  contract  at  the  same  time,  it  is  only  an 
accidental  coincidence. 

The  frequency  and  intensity  with  which  the  contractions  of  each 
single  muscle  ensue  are  not  the  same  on  different  days  or  at  different 
times  of  the  day  noticed.  During  the  times  of  greater  agitation  there 
are  40  to  50  contractions  per  minute  in  one  and  the  same  muscle,  while 
during  the  hours  of  greater  rest  only  10  to  20  contractions  could  be 
counted.  Only  rarely  does  it  happen  that  the  spasm  ceases  entirely,  or 
almost  entirely. 

The  foregoing  is  based  on  Friedreich's  description.  It  corresponds 
with  several  cases  which  I  have  observed  except  that  sometimes  the  trunk 
muscles  are  greatly  involved.  It  seems  to  be  a  toxsemic  disorder,  causing 
an  irritation  of  the  peripheral  motor  neuron.  J.  R.  Hunt  found  hyper- 
trophy of  the  muscular  fibres  in  one  case.  Much  has  been  written  into 
the  original  description  and  some  cases  have  been  classed  as  hysterical, 
but  that  cannot  be  the  pathology  of  the  originally  described  disease.  In 
one  case  observed  by  mj^self  the  muscular  phenomena  were  due  to  a 
general  infection  from  which  death  resulted. 

MYOTONIA 

This  is  the  general  term  given  to  tonic  muscular  spasms,  and  they  may  be  irregular, 
rhythmical,  localized,  or  very  general  in  distribution. 

The  myotonia  may  be  acquired,  and  it  is  then  called  myotonia  acquisita,  or  symp- 
tomatica. Not  much  is  known  of  this  as  a  definite  malady.  It  occurs  sometimes  as  an 
epiphenotnenon  in  progressive  muscular  dystrophy  and  myasthenia  gravis.  It  is  a  not 
uncommon  symptom  of  muscular  exhaustion  or  deficient  vascular  supply. 


544 


DISEASES    OF   THE    NERVOUS    SYSTEM 


Thomsen's  Disease  {Myotonia  Congenita). — This  is  a  hereditary  and  family  disease 
characterized  by  the  development  of  tonic  spasms  when  the  patient  attempts  volun- 
tary movements.     The  disorder  is  very  rare. 

Etiology. — Congenital  myotony  is  practically  always  hereditary  and  runs  in  fami- 
lies.    It  affects  males  by  preference  and  develops  at  the  time  of  adolescence. 

Symptoms. — The  patient  notices  that  on  trying  to  rise  or  walk  his  legs  are  seized 
with  a  painless  spasm,  which  in  a  few  seconds  relaxes,  but  comes  on  again  when  the 
muscular  movements  have  been  repeated.  If  he  closes  his  hands  tightly  a  cramp 
occurs  and  he  cannot  relax  the  grip.  If  he  shuts  his  eyes  he  cannot  open  them  for  a 
moment.     The  muscles  of  mastication  may  be  affected,  but  the  extremities  are  the 


Fig.  234. — Myatonia  congenita.     (Spiller.) 

parts  most  involved.  The  involuntary  muscles  are  spared.  The  spasms  are  increased 
by  cold  and  nervousness;  they  are  lessened  by  muscular  exercise.  The  muscles  are 
somewhat  hypertrophied,  and  the  patient  may  present  the  appearance  of  a  very  strong 
man.  The  actual  strength  is  fair,  but  less  than  would  seem.  The  general  health 
may  be  good,  but  the  patients  sometimes  show  the  signs  of  low  vitality  in  weak  diges- 
tion, feeble  sexual  power,  and  susceptibility  to  cold. 

The  electrical  excitability  of  the  nerves  is  normal,  that  of  the  muscles  is  increased, 
and  there  is  produced  a  contraction  tetanus  by  both  currents.  In  addition,  Erb 
describes  a  peculiar  reaction  produced  by  a  strong  stabile  galvanic  current.  It  con- 
sists in  the  appearance  of  wave-like  muscular  movements  passing  from  cathode  to 


THE    MYOCLONIAS    OR   TWITCHING    SPASMS  545 

anode.     This  is  not  always  present.     The  mechanical  excitability  of  the  muscles  is 
also  increased. 

Pathology. — The  disease  is  probably  a  primary  muscular  dystrophy,  a  view  sup- 
ported by  its  occurrence  in  the  wasting  dystrophies.  There  may  be,  however,  a 
peculiar  defect  in  innervation  resulting  from  a  congenital  anomaly  of  the  motor  tracts. 
The  muscular  fibres  are  found  to  be  hypertrophied,  the  striations  indistinct,  and  the 
nuclei  increased. 

The  diagnosis  is  easily  made  by  the  characteristic  tonic  spasms. 

The  prognosis  is  bad  as  regards  cure,  but  the  disorder  does  not  shorten  life. 

Treatment. — Dr.  Thomsen,  who  first  described  the  disease,  states  that  active 
muscular  exercise  benefits  patients.     No  specific  measures  are  known. 

Symptomatic  Myotonia  and  Paramyotonia. — Paramyotonia  is  the  name  given  to 
a  form  of  myotonia  in  which  the  symptoms  deviate  somewhat  from  the  typical  ones 
that  appear  in  Thomsen's  disease. 

Congenital  paramyotonia  is  a  family  affection,  resembling  in  this  respect  Thomsen's 
disease.  The  muscular  rigidity  is  brought  on  not  by  voluntary  movements,  but  by 
exposure  to  cold  and  often  very  slight  degrees  of  cold.  The  tonic  spasm  is  a  long  one 
and  lasts  for  from  a  quarter  of  an  hour  to  several  hours.  It  affects  the  arms  more 
than  the  legs.  The  facial  muscles  are  prone  to  become  rigid.  The  attacks  are  fol- 
lowed by  some  muscular  weakness.  In  congenital  paramyotonia  the  trouble  is  un- 
doubtedly a  primary  disturbance  of  the  muscles;  in  other  words,  a  myopathy. 

Symptomatic  paramyotonia  is  noted  most  characteristically  in  a  certain  form  of 
paralysis  agitans.  Here  the  patient,  when  attempting  to  walk  or  to  rise  from  the 
sitting  posture,  is  suddenly  seized  with  an  apparent  rigidity  of  the  muscles  which  pre- 
vents him  from  stirring.  The  trouble  is  probably  more  central  than  muscular.  The 
myotonic  condition  appears  in  the  progressive  muscular  dystrophies,  and  in  spastic 
paralyses  of  spinal  and  cerebral  origin. 

Ataxic  paramyotonia  is  the  name  given  to  a  disorder  characterized  by  transient 
spasms  like  those  of  Thomsen's  disease,  associated  with  distinct  ataxia  and  also  with 
weakness  and  some  anaesthesia  (Gowers).  This  disease  is  probably  located  in  the 
spinal  cord  and  should  perhaps  be  considered  one  of  the  forms  of  symptomatic  para- 
myotonia. No  special  treatment  can  be  given  for  either  of  the  two  latter  forms  of 
disease,  of  which  very  few  examples  have  been  observed. 

Hypotonia  and  Myatonia.- — A  few  cases  have  been  observed  in  which  from  birth 
the  muscles  have  shown  a  pe)sistent  and  extreme  hypotonia.  This  forms  a  condition 
known  as  congenital  myatonia  (Fig.  234).  It  is  thought  by  some  to  be  a  fo'm  of 
dystrophy.  Minor  degrees  of  myatonia  occur  in  many  people  and  are  not  to  be  re- 
garded as  morbid  conditions.  Hypotonia  is  more  marked  generally  in  the  female  sex, 
and  it  is  developed  by  acrobats  and  freaks.  It  exists  as  one  of  the  symptoms  of 
Mongolian  idiocy. 

TORTIPELVIS 

{Dystonia  Musculorum  Deformans) 

Cases  of  this  curious  disease  have  been  described  by  several  American 
neurologists,  notably  by  Dr.  J.  Fraenkel  who  called  it  tortipelvis.  Oppen- 
heim  has  described  it  under  the  name  if  dystonia  musculorum  deformans. 
It  is  a  functional  myotonic  disorder  characterized  by  peculiar  tonic 
spasms  of  the  muscles  of  the  trunk  and  pelvic  girdle,  which  are  brought 
out  especially  on  attempting  to  walk.  The  disease  develops  in  early  life, 
affects  both  sexes  and  various  races.     It  is  chronic  in  its  course. 

35 


546 


DISEASES    OF    THE    NERVOUS    SYSTEM 


When  the  patient  attempts  to  walk  his  trunk  and  thigh  muscles  are 
seized  with  slow,  irregular,  tonic  and  sometimes  clonic  spasms,  which 
bend  the  body  forward,  sideways,  and  twist  it.  The  effect  is  to  produce 
an  awkward  and  grotesque  and  so-called  ''dromedary"  gait.  The  legs 
also  are  involved  in  the  spasms,  the  neck  and  arms  but  slightly  (Fig. 
235).     When  the  patient  lies  down  or  sits  quietly  the  spasms  cease  to 

an  extent,  but  begin  again  when 
he  attempts  voluntary  movements. 
There  are  no  disturbances  of  sen- 
sation or  of  the  reflexes.  The  mind 
is  clear. 

The  spasms  are  much  like  the 
myotonia  of  spasmodic  tic.  The 
physiognomy  of  the  disease,  its  re- 
sponse in  a  degree  to  pedagogical 
treatment,  the  absence  of  all  evi- 
dences of  organic  disease  all  sug- 
gest that  the  malady  is  allied  to  the 
spasmodic  tics. 

TETANUS 

Tetanus  is  an  acute  or  sub- 
acute infectious  disease  character- 
ized by  violent  and  painful  tonic 
spasms  with  remissions  and  exacer- 
bations. It  is  due  to  infection  by 
the  tetanus  bacillus.  It  is  called 
idiopathic  or  medical  tetanus  when 
no  open  wound  is  found  and  trau- 
matic or  surgical  tetanus  when 
such  condition  is  present.  When 
it  attacks  infants  it  is  called  tet- 
anus neonatorum;  when  the  jaws 
alone  are  involved  it  is  called  lock- 
jaw, or  trismus.  A  form  which  af- 
fects the  face  and  throat  is  called 
head  or  cephalic  tetanus.  The  idiopathic  or  medical  tetanus  is  more 
chronic  in  its  course. 

Etiology. — It  has  a  special  predilection  for  newborn  children  in  some 
countries  (West  Indies)  and  to  a  less  extent  for  puerperal  women.  It 
affects  males  more  than  females  (4  to  1).  After  the  first  month  of  life 
there  is  practical  immunity  till  after  the  tenth  year.  It  then  increases  in 
frequency  to  about  thirty.     Most  cases  occur  between  the  fifth  and 


Fig.  235. — Torti  pelvis — Dystonia  mus- 
culorum.    {Dj-.  Goodhart.) 


THE    MYOCLONIAS    OR    TWITCHING    SPASMS  547 

twenty-fifth  year  (Anders).  It  is  rare  after  forty  to  fifty.  It  is  much 
more  frequent  in  dark  races  and  in  some  tropical  cHmates  (West  Indies, 
South  and  Central  America).  It  is  more  frequent  in  some  regions  of  the 
temperate  zone  than  others  because  of  an  infected  soil.  It  is  more  com- 
mon in  hot  seasons. 

It  is  caused  generally  by  traumatism,  and  most  often  by  contusions 
and  penetrating  soil  infected  wounds  of  the  hands  and  feet,  hence  its 
prevalence  in  times  of  war.  In  cephalic  tetanus  there  is  traumatism  of 
this  extremity.  In  this  country  traumatism  of  the  hands  on  Fourth  of 
July  causes  many  cases. 

Symptoms. — The  disease  sets  in  from  five  to  fifteen  days  after  infec- 
tion. It  begins  with  feelings  of  stiffness  in  the  neck  and  throat  and  some- 
times with  chilly  feelings.  Gradually  tonic  spasms  develop  which  involve 
the  trunk  and  head  muscles,  causing  opisthotonos  and  other  forms  of 
rigid  spasm.  Trismus,  or  lockjaw,  also  occurs.  The  spasms  are  attended 
with  intense  pain.  The  patient  finally  lies  in  a  state  of  general  rigidity 
interrupted  by  painful  tonic  spasms.  The  muscles  are  of  stony  hardness. 
The  jaws  are  set  and  the  facial  muscles  are  involved,  the  eyes  being  partly 
closed,  the  corners  of  the  mouth  drawn  up,  causing  the  characteristic 
risus  sardonicus.  There  may  be  profuse  sweating;  some  leukocytosis  is 
present;  tissue  metabolism  is  not  much  changed.  Fever  is  generally 
present  and  this  may  rise  as  death  approaches  to  110°  or  112°.  The 
disease  lasts  from  two  to  five  weeks.  There  is  evidence  of  irritation  and 
congestion  of  the  spinal  cord  and  injured  nerves,  but  no  special  anatomical 
changes  are  found.  A  specific  bacillus  producing  a  tetanizing  poison  has 
been  discovered,  the  bacillus  tetani. 

The  diagnosis  is  based  on  the  characteristic  history  and  the  peculiar 
spasms.  In  strychnine  poisoning  there  is  no  initial  trismus  or  epigastric 
pain.  In  rabies  there  is  also  no  trismus,  but  a  respiratory  spasm  on  at- 
tempts to  swallow. 

The  prognosis  is  bad.  About  80  per  cent,  of  traumatic  and  40  per 
cent,  of  slow  idiopathic  cases  die. 

The  treatment  consists  of  complete  rest  and  quiet  in  a  dark  room  and 
the  adminsitration  of  chloral,  bromide,  morphine,  and  physostigma. 
Successful  results  from  injection  of  blood-serum  of  an  animal  which  has 
had  the  disease  are  reported.  A  tetanus  ''vaccine"  has  been  obtained 
and  lately  used  viiih  success.  This  must  be  administered  both  intra- 
spinally  and  intravenously  in  maximum  doses. 

TETANY 

(Tetanilla) 

Tetany  is  a  subacute  or  chronic  spasmodic  disorder  characterized  by  intermittent 
or  persistent  tonic  contractions  beginning  in  the  extremities  and  associated  with 
paraisthesiffi  and  hyperexcitability  of  the  motor  and  sensory  nerves. 


548  DISEASES    OF    THE    NERVOUS    SYSTEM 

Etiology. — The  disease  is  rare  in  this  country,  but  relatively  common  in  Europe, 
especially  in  Austria.  It  occurs  with  frequency  during  the  second,  third,  and  fourth 
years  of  life  and  again  at  the  time  of  puberty.  Its  rate  of  frequency  then  slowly 
declines  and  it  is  very  rare  after  fifty.  It  affects  males  much  oftener  than  females 
up  to  the  age  of  twenty;  after  that  the  difference  disappears.  It  occurs  mostly  in  the 
working  classes.  In  infants  rickets  is  often  noted.  The  exciting  causes  are  exhaust- 
ing influences  like  diarrhoea,  lactation,  sepsis,  fatigue,  mental  shock,  and  fevers; 
also  exposure  to  cold  and  wet.  Alcoholism,  dilatation  of  the  stomach,  and  intestinal 
entozoa  are  also  causes.  It  may  be  produced  artificially  by  extirpation  of  the  para- 
thyroid gland.     The  disease  sometimes  appears  as  an  epidemic. 

Symptoms. — Tetany  begins  sometimes  suddenly  with  symmetrical  tonic  contrac- 
tions of  the  hands;  at  other  times  there  are  at  first  sensations  of  numbness,  prickling 
or  pain  in  the  extremities,  with  malaise  and  perhaps  nausea;  then  spasms  begin.  The 
attacks  affect  first  and  most  the  upper  extremities.  The  flexors  of  the  forearm  and 
hand  are  usually  involved;  the  fingers  are  flexed  at  the  metacarpo-phalangeal  joint  and 
extended  at  the  other  joints,  and  the  thumb  is  adducted,  producing  the  "accoucheur's 
hand."     The  forearm  may  be  flexed  and  the  upper  arm  adducted.     The  knees  and 


Fig.  236. — The   Trousseau  symptom. 

feet  are  extended,  the  toes  flexed,  and  the  foot  is  inverted.  In  severe  cases  the  muscles 
of  the  abdomen,  chest,  neck,  and  face  are  involved.  Opisthotonos  and  dyspnoea  may 
result.  The  muscles  of  the  face  and  eyes  develop  contractions,  and  trismus  sometimes 
occurs  late  in  the  disease.  The  muscles  of  the  larynx,  oesophagus  and  bladder  may  be 
affected.  Fibrillary  tremors  are  observed  in  the  contracted  muscles.  The  attacks 
are  accompanied  by  parsesthesias  and  cramp-like  pains.  There  may  be  some  aboli- 
tion of  sensation  in  the  skin  of  the  parts  affected  during  attacks.  The  cramps  last 
from  a  few  minutes  to  hours  or  days.  They  occur  during  day  and  night  and  may  wake 
the  patient  from  sleep.  Fever  is  sometimes  present  in  epidemic  cases.  The  disease 
has  a  tendency  to  recurrence. 

While  it  lasts,  both  during  and  between  the  attacks,  peculiar  phenomena  are  ob- 
served as  follows: 

1.  Increased  Mechanical  Irritability  of  Motor  Nerves. — The  motor  nerves  show 
an  abnormal  irritability,  so  that  on  striking  the  motor  point  a  sharp  muscular  contrac- 
tion is  brought  out.  When  pressure  or  a  blow  is  made  on  the  face  over  or  near  the 
exit  of  the  facial  nerve  from  its  foramen,  contractions  of  the  facial  muscles  occur,  es- 
pecially those  of  the  lips.  This  is  called  the  "facial  phenomenon."  By  pressing  on 
the  artery  and  nerve  of  a  limb  a  tetanic  attack  can  be  produced  in  the  muscles  supplied. 


THE    MYOCLONIAS    OR   TWITCHING    SPASMS 


549 


It  is  probable  that  it  is  the  pressure  on  the  nerve  alone  which  causes  the  phenomenon 
which  is  called  "Trousseau's  symptom"  (Fig.  236) 

2.  The  electrical  irritability  of  the  muscles  and  nerves  is  increased,  especially  to 
the  galvanic  current.  Thus  a  negative-pole  closure  contraction  (CaCC)  is  brought  out 
by  a  very  weak  current;  and  if  a  little  stronger  it  causes  a  tonic  contraction  or  cathode- 


FiG.  237. — The  parathyroids.     {Halstead  and  Evans.) 


closure  tetanus  (CaCTe).  The  positive-pole  opening  contraction  (AnOC)  may  be 
tetanic,  i.e.,  AnOTe,  and  there  may  be  even  a  cathode-opening  tetanus  (CaOTe),  a 
phenomenon  not  seen  in  any  other  disease.  According  to  Gowers  there  may  be  a 
reversal  of  the  polar  formula,  so  that  a  positive-pole  closure  contraction  occurs  earlier 
than  a  negative  (AnCC>CaCC).     This  is  certainly  rare. 


550  DISEASES    OF    THE    NERVOUS    SYSTEM 

3.  An  increase  of  irritability  of  the  sensory  nerves  is  shown  by  pressing  upon  them, 
when  sensations  of  prickhng  and  formication  appear  along  their  course.  There  is  an 
increase  also  in  the  electrical  sensibility,  shown  by  appreciation  of  very  weak  galvanic 
currents.  The  auditory  nerve  reacts  to  the  galvanic  current  in  about  15  per  cent, 
of  normal  cases,  and  then  only  to  strong  currents  and  to  only  a  partial  extent;  but  in 
tetany  it  reacts  in  nearly  all  cases,  and  with  comparatively  weak  currents  (2  to  5  or 
6  ma.)  on  anode  closure,  anode  fixed,  and  anode  opening  (AnC  Klang,  AnDKl,  AnOKl) 
(Chvostek). 

The  phenomena  of  hyperexcitability  above  described  vary  considerably  and  rapidly 
during  the  course  of  the  disease,  and  are  not  always  present. 

Types  of  the  Disease. — The  disease  varies  in  intensity  and  duration.  This  varia- 
tion depends  much  upon  the  cause,  and  there  have  been  a  number  of  types  of  the  dis- 
ease based  on  the  etiology.     Thus  we  have: 

1.  Epidemic  tetany. 

2.  Asthenic  tetany  due  to  lactation,  diarrhoea,  exhausting  diseases,  etc. 

3.  Parathyroid  tetany,  due  to  removal  of  the  parathyroid  glands. ^ 

4.  Reflex  and  toxic  tetany  from  gastric  dilatation  and  intestinal  worms. 

When  the  spasms  are  continuous  the  disease  lasts  but  a  few  weeks;  when  they  are 
intermittent  it  may  continue  for  months.  Epidemic  cases  last  but  a  few  weeks.  The 
disease  may  be  said  in  general  to  last  from  a  few  weeks  to  a  few  months.  It  is  rarely 
fatal.     Patients  are  liable  to  a  recurrence  on  return  of  the  exciting  cause. 

Pathology. — The  phenomena  of  the  disease  indicate  a  congested  and  irritative 
condition  of  the  gray  matter  of  the  spinal  cord.  The  cause  of  this  state  is  evidently 
in  some  cases  (epidemic  tetany)  an  infectious  poison;  in  other  cases  as  auto-toxin  in 
the  blood  (parathyroid  tetany),  and  in  other  cases  it  may  be  a  rheumatic  or  some  other 
toxic  influence.     Ergot  is  known  to  produce  symptoms  resembling  tetany. 

In  infantile  tetany  the  irritation  is  apparently  due  to  rickets  and  the  reflex  irrita- 
tion of  disordered  bowels.  It  is  doubtful  if  any  reflex  influence  can  be  invoked  in 
adults.  Tetany  is  a  functional  disease  and  the  symptomatic  expression  of  a 
toxaemia.  This  poison  may  be  of  different  kinds,  hence  tetany  has  a  claim 
to  be  called  a  distinct  disease  simply  on  clinical  grounds.  It  has  no  such  definite 
pathology  as  chorea  or  epilepsy.  In  the  very  few  autopsies  which  have  been  made  no 
definite  organic  lesion  has  been  found. 

Diagnosis. — -The  disease  is  usually  easily  recognized  by  the  character  of  the  spasms, 
their  symmetrical  nature,  their  course,  and  the  phenomena  of  hyperexcitability  of  the 
muscles  and  nerves.  Trousseau's  symptom  is  found  in  no  other  disease.  The  "facial 
phenomenon,"  the  peculiar  electrical  and  mechanical  irritability  of  the  muscles  and 
nerves,  are  very  rare  in  other  conditions.  The  sensory  irritability,  especially  that 
of  the  acoustic  nerve,  is  also  characteristic.  From  tetanus  the  disease  is  distin- 
guished by  the  intermittency  of  the  contractions,  their  feebler  character,  the  fact 
that  they  begin  in  the  extremities  and  extend  to  the  trunk,  and  by  the  absence  of 
trismus,  at  least  until  late  in  the  disease. 

Treatment. — ^The  cause  should  be  removed  if  possible,  lactation  stopped,  diarrhoea 
and  indigestion  corrected,  the  stomach  washed  out,  worms  expelled,  rickets  if  present 

1  A  distinct  form  of  tetany  is  due  to  disease  of  or  removal  of  the  parathyroid  glands. 
It  is  believed  that  when  tetany  follows  operations  upon  the  thyroid  gland  itself,  it  is 
due  to  the  removal  of  one  or  more  of  the  parathyroids.  These  glands  are,  in  human 
beings,  very  small  objects — about  half  the  size  of  a  pea,  four  in  number-;-the  upper 
pair  and  the  lower  pair;  and,  according  to  Dr.  Halstead,  they  have  a  definite  vascular 
supply.  In  cases  of  tetany,  due  to  partial  or  complete  removal  of  these  glands,  the 
tetany  can  be  kept  under  control  by  feeding  the  patients  with  these  glands  or  the  nucleo- 
proteid  obtained  from  them. 


THE    MYOCLONIAS    OR    TWITCHING    SPASMS  551 

attended  to.  Rest,  nourishing  food,  and  tonics  are  indicated.  Symptomatically, 
bromide  of  potassium  in  doses  of  5iss.  to  3ij-  daily  with  chloral  furnishes  the  surest 
relief.  Hyoscine  in  doses  of  gr.  Jd^oo  may  be  tried.  Inhalation  of  chloroform  or  in- 
jections of  morphine  are  needed  in  severe  cases.  Lukewarm  baths  may  be  of  service; 
so  also  may  ice  bags  to  the  spine.  Parathyroid  feeding  or  injection  of  the  nucleo- 
proteid  should  be  tried. 

RABIES  AND  HYDROPHOBIA 

Rabies  is  an  acute  specific  disease,  communicated  to  man  from  the 
lower  ammals,  and  characterized  by  severe  and  painful  tetanic  convul- 
sions, paralysis  and  death.  The  disease  occurs  in  nearlj^  all  parts  of  the 
world,  and  is  common  throughout  the  United  States.  All  mammals  are 
susceptible  to  the  disease,  and  birds  also  may  contract  it. 

Etiology. — The  commonest  source  of  infection  is  the  bite  of  a  dog; 
but  the  disease  may  be  caused  by  the  bite  of  cats,  wolves,  horses,  cattle, 
and  other  domestic  animals.  The  bites  of  wolves  are  the  most  dangerous, 
next  those  of  cats,  and  next  those  of  dogs.  It  is  not  communicated  by 
the  bite  of  a  rabid  man.  Bites  upon  the  face  and  hands,  the  exposed 
parts  of  the  body,  are  more  dangerous  on  account  of  the  rich  nervous 
supply  and  from  the  lack  of  the  protection  of  the  clothing.  The  disease 
may  be  transmitted  by  saliva  upon  an  abraded  surface.  About  one- 
sixth  of  persons  who  are  bitten  by  rabid  dogs,  become  infected.  Men  are 
more  susceptible  than  women,  and  nearly  half  of  the  cases  occur  in  persons 
under  20.  Rather  more  cases  occur  during  the  months  from  April  to 
September.  The  infection  is  contained  in  the  saliva,  and  is  secreted 
mainly  by  the  parotid.  Other  glands  may  contain  it,  and  it  may  be 
excreted  in  the  milk.  The  blood  and  lymph  are  never  virulent.  In 
the  infected  person  the  virus  pervades  every  part  of  the  central  nervous 
system,  but  is  especially  concentrated  in  the  medulla.  It  exists  also  in 
the  cerebrospinal  fluid  and  large  nerve  trunks. 

The  microbe  of  rabies  has  not  been  discovered.  Whatever  it  is,  it 
makes  its  way  into  the  nervous  system,  along  the  nerve  trunks.  It  has 
an  incubation  period  of  about  fort}^  days,  ranging  between  twenty  and 
ninety  days. 

The  characteristic  histological  change  in  rabies  is  certain  bodies  dis- 
covered in  the  nerve-cells  by  Negri.  They  are  called  the  Negri  bodies. 
These  are  not  easily  affected  by  external  agencies,  even  by  putrefaction, 
and  are  easily  stained  and  observed  under  the  microscope.  By  means 
of  observing  these  bodies,  the  diagnosis,  after  death,  of  the  disease  is  very 
easily  made. 

The  Negri  bodies  are  specific  of  rabies,  and  they  have  been  thought 
to  be  protozoa.  This  has  not  been  proved,  and  it  is  still  most  probable 
that  the  virus  of  rabies  is  an  ultramicroscopical  body  which  is  in  some 
way  connected  with  tissue  proteids  which  form  the  Negri  bodies. 


552  DISEASES    OF    THE    NERVOUS    SYSTEM 

Symptoms. — As  a  rule,  there  are  no  symptoms  during  the  incubation 
period.  When  the  disease  develops,  there  is  some  numbness,  tingling, 
and  perhaps  radiating  pain  at  the  point  where  the  bite  occurred.  The 
person  suffers  from  nervousness,  anxiety  and  depression;  the  sleep  is  dis- 
turbed, and  then  some  symptoms  referable  to  the  throat  appear.  There 
is  early  a  difficulty  in  swallowing.  In  a  few  days  the  symptoms  of  mental 
excitement  appear.  The  patient  becomes  more  restless,  nervous  and 
insomnolent.  He  suffers  from  thirst,  but  cannot  quench  it,  because  at- 
tempts to  drink  cause  a  painful  spasm  of  the  throat.  As  a  result,,  while  he 
desires  to  drink,  the  sight  of  water  frightens  and  distresses  him.  Hence, 
the  name  hydrophobia.  Then  he  begins  to  have  attacks  of  convulsions, 
which  affect  first  the  muscles  of  the  neck  and  throat  and  then  involve 
the  whole  body,  causing  symptoms  resembling  tetanus.  At  other  times, 
there  are  very  active  co-ordinated  convulsions,  like  those  of  hysteria. 
Slight  sounds  or  any  mental  excitement  will  bring  on  an  attack.  De- 
lirium and  maniacal  excitement  complicate  the  condition,  which  lasts  from 
one  to  three  days.  A  general  paralysis  follows,  and  the  patient  dies  in 
coma,  from  exhaustion,  the  temperature  rising  quite  high.  In  cases 
where  the  infection  is  very  severe,  the  system  is  overwhelmed  by  the  virus, 
and  the  patient  dies  very  quickly  with  an  ascending  paralysis  which  re- 
sembles a  so-called  Landry's  paralysis  (paralytic  rabies). 

Diagnosis. — -In  the  early  stages  of  the  disease,  the  mental  condition 
of  the  patient  and  the  convulsive  attacks  are  very  suggestive  of  acute 
hysteria.  The  history  of  a  bite  and  the  person's  respiratory  spasms  and 
throat  spasms  will  generally  exclude  this.  In  tetanus,  there  is  more  or 
less  continuous  rigid  spasm  between  the  attacks;  the  history  of  the  disease 
and  the  longer  period  of  incubation  in  rabies  enable  us  to  distinguish  it. 

Prognosis. — ^When  the  disease  comes  on,  the  issue  is  surely  a  fatal 
one.  The  careful  application  of  the  Pasteur  treatment,  by  inoculation, 
reduces  the  mortality  after  bites  from  about  16  to  one-half  of  1  per  cent. 

The  treatment  after  the  attack  comes  on  is  purely  symptomatic,  and 
consists  in  the  use  of  morphine,  chloroform  and  motor  depressants,  such 
as  curare. 


CHAPTER  XXV 

EXOPHTHALMIC    GOITRE    (FAJANPS   DISEASE,   GRAVES'   DIS- 
EASE, BASEDOW'S  DISEASE)  AND  HYPERTHYROIDISM 

Exophthalmic  goitre  is  a  chronic  glandular  neurosis  characterized  by 
easy  fatigability,  rapid  heart  beat,  enlargement  of  the  thyroid  gland, 
protrusion  of  the  eyeballs,  tremor,  and  various  neurasthenic,  metabolic 
and  vasomotor  symptoms. 

Etiology.— Exophthalmic  goitre  occurs  much  oftener  in  women  than 
men  (four  to  one).  It  is  a  disease  of  early  adult  life,  occurring  chiefly 
between  fifteen  and  thirty-five,  very  rarely  in  childhood,  and  never  after 
fifty.  It  is  apparently  more  common  in  the  Anglo-Saxon  race,  but  is  not 
very  frequent  in  America,  at  least  in  the  Eastern  States.  I  am  informed 
that  it  is  rather  common  in  the  Northern  Central  States.  There  is  very 
rarely  any  direct  inheritance  of  the  disease,  but  the  family  is  often  a 
neuropathic  one.  As  a  rule,  the  patient  is  of  a  neurotic  temperament. 
Anaemia  and  debilitating  diseases  promote  its  development.  Syphilis  is 
rarely  present,  and  probably  not  a  cause.  Goitre  and  heart  disease  do 
not  seem  to  predispose  to  the  real  trouble,  but  a  goitre  may  lead  to  a 
symptomatic  Graves'  disease  characterized  mainly  by  cardiac  disturb- 
ances and  perhaps  some  cervical  sympathetic  symptoms.  The  most 
frequent  exciting  causes  are  powerful  and  depressing  emotions  and  severe 
physical  exertion.  Rarer  causes  are  injuries  and  infectious  diseases, 
such  as  influenza,  measles,  scarlet  fever,  typhoid  fever,  and  pneumonia. 
It  sometimes  develops  after  such  infections  without  any  previous  nervous 
strain  or  shock.     I  have  met  no  cases  following  directly  upon  traumatism. 

HYPERTHYROIDISM 

The  symptoms  grouped  under  the  term  exophthalmic  goitre  represent 
a  phase  in  the  pathological  history  of  the  thyroid  gland.  When  this  gland 
is  atrophied  and  inactive  we  have  hypothyroidism  and  myxoedema;  when 
over-active,  hyperthyroidism  and  exophthalmic  goitre.  Qualitative 
changes  occur  in  which  hyper-  and  hypo-symptoms  are  mingled. 

Exophthalmic  goitre,  according  to  Rogers,  may  be  preceded  by  hypo- 
thyroidism, this  may  be  followed  by  hyperthyroidism,  and  finally  the 
fully  developed  type  of  exophthalmic  goitre  appears. 

Hyperthyroidism  is  a  not  infrequent  condition,  and  is  characterized 
by  nervousness,  emotional  weakness,  a  kind  of  hypo-manic  restlessness, 

553 


554  DISEASES    OF    THE    NERVOUS    SYSTEM 

insomnia,  fatigability,  moist  skin,  tendency  to  palpitations,  and  other 
of  the  minor  vasomotor  and  secretory  symptoms  of  Graves'  disease. 
The  condition  may  go  no  farther  than  such  hyperthyroid  state,  or  it  may 
eventuate  in  the  final  and  more  definite  disease. 

Symptoms. — The  disease  usually  begins  gradually,  and  the  first  symp- 
tom is  in  most  cases  rapid  heart  beat,  associated  with  attacks  of  palpita" 
tion.  The  patient  is  nervous,  easily  fatigued,  and  has  sometimes  tremor. 
The  next  symptom  is  enlargement  of  the  thyroid  gland,  and  at  about 
the  same  time  the  eyeballs  begin  to  protrude.  This  order  of  develop- 
ment does  not  always  take  place,  and  occasionally  one  or  more  of  the  five 
principal  symptoms  is  not  present. 

The  disease  is  usually  one  or  two  years  in  developing,  the  heart  symp- 
toms being  those  which  begin  first  and  end  last.  With  the  symptoms 
above  mentioned  there  occur  many  minor  troubles  which  are  more  or  less 
characteristic.  The  patient  is  usually  very  nervous  and  irritable;  a  dis- 
tressing insomnia  may  be  present.  There  is  almost  uniformly  a  fine 
tremor  (eight  to  nine  per  second)  of  the  hands,  less  marked  in  the  lower 
limbs  and  not  present  in  the  face  or  tongue.  The  reflexes  are  exaggerated. 
There  is  a  tendency  at  times  in  walking  for  the  knees  suddenly  to  give 
way.  The  patient  rarely  has  neuralgias,  but  does  have  burning  or  fever- 
ish sensations  and  headaches.  The  skin  is  rather  reddened  and  moist, 
and  the  patient  at  times  sweats  profusely.  Pigmentation  and  vitiligo 
are  sometimes  seen,  and  urticaria  may  develop.  The  electrical  resistance 
of  the  body  is  much  diminished,  being  800  to  1,500  ohms  instead  of  2,000 
to  3,000.  There  is  sometimes  a  dermographic  skin,  as  in  other  neuras- 
thenic states.  The  respiratory  function  is  weakened  and  chest  expansion 
often  falls  below  one  inch  (Fiske-Bryson) .  Attacks  of  a  persistent  watery 
diarrhoea  occur.  Anaemia  is  usually  present.  There  is  occasionally 
polyuria,  more  rarely  glycosuria.  A  study  of  the  urine  shows  an  increase 
in  general  metabolic  activity.  The  menses  are  irregular  and  amenorrhoea 
often  exists.     A  slight  rise  in  temperature  may  occur. 

The  blood-pressure  varies  but  eventually  is  somewhat  increased. 
The  major  symptoms  of  the  disease  are: 

Mental  and  physical  fatigue. 

Tachycardia. 

Goitre. 

Exophthalmus. 

Tremor. 
The  minor  symptoms  are: 

Nervousness. 

Sweating. 

Insomnia. 

Lessened  electrical  resistance. 


EXOPHTHALMIC    GOITRE 


555 


Subjective  sensations  of  heat. 

Diarrhoea. 

Polyuria . 

Increased  metabohsm. 
The  sense  of  fatigue,  and  the  easy  fatiguability  have  been  dwelt  upon 
correctly  by  Rogers,  as  a  fundamental  symptom.     It  is  practical^  the 
same  condition  as  that  found  in  neurasthenia  proper.     Next  to  this  and 
as  common,  is  the  symptom  of  tachycardia. 

Symptoms  in  Detail. — The  pulse  beats  from  100  to  120  per  minute 
usually,  but  may  rise  to  160  or  even  200.  Its  rhythm  is  usually  steady; 
but  palpitations  occur  easily,  even  without  exciting  cause.  The  patient 
may  wake  up  at  night  with  distressing  attacks,  something  like  those  of 
angina  pectoris,  but  the  intense  pain  and  sense  of  imioending  death  are 


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Fig.  238. — Exophthalmic  goitre. 

usually  absent.  The  heart  is  dilated  and  a  systolic  murmur  is  often 
heard  at  the  base  propagated  along  the  arteries.  Real  organic  disease, 
however,  is  rare.  The  arteries  are  dilated  and  soft.  They  pulsate 
strongly,  particularly  the  carotids.  A  thrill  is  sometimes  felt  over  the 
heart  and  always  over  the  goitre.  The  arterial  tension  is  normal  or  low 
at  first;  later  it  is  high. 

The  thyroid  gland  is  usually  enlarged  symmetrically;  later  in  the  dis- 
ease the  isthmus  is  affected  and  the  three  lobes  of  the  gland  stand  out 
prominently  (Fig.  238).  If  only  part  of  the  gland  is  involved  it  is  oftenest 
the  right  lobe.  A  thrill  is  felt  over  it  and  a  systohc  murmur  can  be  heard. 
The  enlargement  of  the  thyroid  is  slight  or  not  detectable  in  a  small  per 
cent,  of  cases. 

The  bulging  of  the  eyes  or  exophthalmus  is  usually  bilateral  and  even. 


556  DISEASES    OF    THE    NERVOUS    SYSTEM 

If  one  eye  is  alone  or  more  affected  it  is  the  right.  The  exophthalmus 
varies  much  in  degree.  It  is  not  usually  very  great,  but  may  be  so  ex- 
cessive as  to  prevent  closing  of  the  lids  and  to  expose  the  insertions  of  the 
recti.  The  eyeball  may  be  slightly  enlarged  (one-tenth) .  The  exoph- 
thalmus is  due  to  the  overaction  of  certain  muscular  bands  which  lie  in 
the  orbit  (Miller's  muscle) ;  also  to  stimulation  of  the  superior  tarsal 
muscle  which  retracts  the  upper  lid.  These  muscles  are  under  the  in- 
fluence of  cervical  sympathetic,  and  not  the  autonomic  fibres.  The 
orbital  space,  as  the  eye  is  pulled  forward,  is  gradually  filled  by  fat 
and  connective  tissue.  Hence  section  of  the  cervical  sympathetic  does 
not  lead  to  more  than  a  slight  relief  of  the  exophthalmus.  The  pupils 
are  normal  and  vision  is  not  impaired,  though  myopia  occasionally 
occurs.  The  fundus  and  visual  field  are  normal.  Paralysis  of  some 
of  the  eye-muscles  is  a  rare  complication.  Weakness  of  the  internal 
recti  and  exophoria  are  frequent.  The  inability  to  converge  the  eyes 
is  known  as  Moehius'  symptom.  The  lids  show  certain  peculiarities. 
One  of  these,  known  as  Von  Graefe's  symptom,  consists  in  the  inability 
of  the  lid  to  follow  the  downward  movement  of  the  eyeball.  When 
the  patient  is  told  to  follow  the  movement  of  the  finger  vertically 
downward  the  eyeball  moves  steadily,  but  the  lid  catches,  as  it  were, 
and  refuses  to  follow  or  does  so  in  a  jerky  manner.  Another  symptom, 
known  as  Stellwag's  symptom,  is  the  widely  open  eye,  showing  white 
around  the  iris  with  infrequency  in  winking,  especially  of  the  upper  lid. 
A  tremor  of  the  lids  sometimes  occurs. 

Course. — The  disease  progresses  slowly.  After  a  year  or  two  it 
often  becomes  stationary  for  a  long  time.  Cases  of  gradual  spon- 
taneous recovery  occur.  The  natural  duration  of  most  recoverable 
cases  is  two  or  four  years.  In  those  which  do  not  recover,  the  disease 
lasts  five,  ten,  or  more  years;  the  patient  emaciates,  the  heart  becomes 
weaker,  albuminuria  and  dropsy  appear,  diarrhoea  sets  in,  and  the 
patient  dies  of  exhaustion  or  is  carried  off  by  phthisis  or  some  inter- 
current disease.  Other  cases,  having  improved  up  to  a  certain  point, 
remain  in  this  state  for  years. 

Complications. — Mental  derangement  occasionally  occurs  in  the 
later  stages  of  the  disease.  Hysterical  crises,  epileptic  attacks,  choreic 
movements,  paralysis  of  the  ocular  muscles,  muscular  atrophy,  paralysis 
agitans,  Addison's  disease,  diabetes,  locomotor  ataxia,  and  local  oedema 
have  all  been  observed.  With  the  exception  of  hysterical  attacks,  these 
complications  are  rare. 

Abortive  Forms. — ^This  name  is  applied  to  cases  in  which  only  a  part 
of  the  distinctive  symptoms  develop.  It  generally  means  hyperthy- 
roidism with  some  of  the  major  symptoms  of  exophthalmic  disease. 
Tachycardia  always  exists;  with  it  are  tremor  and  moist  skin,  lessened 


EXOPHTHALMIC    GOITRE  557 

electrical  resistance  and  nervousness.     Or  tachycardia  and  goitre  may 
alone  be  present. 

Physiology. — ^The  bio-chemical  studies  of  the  thyroid  shows  that  it 
develops  certain  peculiar  iodinized  proteids  which  are  characteristic  of 
its  secretory  activity.  The  exact  nature  of  the  substances  is  not  perfectly 
known.  The  action  of  the  thyroid  is  to  stimulate  metabolism,  and  in- 
directly to  promote  certain  functional  activities.  Its  secretion  seems 
necessary  for  the  growth  and  development  of  all  the  tissues.  The  thyroid 
has  a  certain  interrelation  with  the  pancreas,  adrenals,  thymus  and 
pituitary. 

Pathological  Anatomy. — ^Post-mortem  examination  of  the  thyroid 
gland  shows  that  it  undergoes  a  true  hypertrophy  with  increase  of  vas- 
cularity and  of  the  glandular  structure,  and  increase  of  colloid  material 
in  the  alveoli.  After  the  hypertrophy  has  reached  a  certain  stage,  the 
glandular  epithelium  degenerates  and  breaks  down,  filling  the  acini  with 
degenerated  cells.  Later  still  there  may  be  atrophy  and  fibrosis  with 
sclerosis  of  the  vessels,  hemorrhages  and  cyst  formation. 

In  the  nerve-centres  the  changes  which  have  been  found  are  small 
hemorrhages  in  the  medulla  and  degenerated  nerve-cells.  In  one  case 
of  about  a  year's  standing,  I  found  a  very  marked  pigmentation  and 
vacuolization  of  the  cells  of  the  vagus  and  glossopharyngeal  nuclei. 
In  another  case  of  six  months'  standing,  no  marked  changes  could  be 
seen  in  these  areas,  but  there  was  a  spot  of  softening  at  the  junction 
of  the  pons  and  the  cerebral  peduncle.  This  was  ante-mortem  and 
had  led  to  crossed  paralysis  just  a  few  days  before  death.  In  other  cases 
congestion  and  small  hemorrhages  in  the  medulla  have  been  found. 
In  still  other  cases  there  were  no  lesions,  so  that  an  actual  anatomical 
change  in  the  nervous  centres  cannot  be  said  to  be  established.  The 
heart  is  dilated  and  enlarged;  endocarditis  is  sometimes  present,  oftener 
not;  the  arteries  are  dilated. 

Pathology. — Some  writers  now  consider  this  disease  primarily  one 
due  to  a  disordered  function  of  the  thyroid  gland.  This  is  not  entirely 
the  case.  Graves'  disease  occurs  in  neuropathic  persons.  It  is  often 
associated  with  a  neuropathic  family  history  and  often  neuroses  compli- 
cate the  thyroid  trouble.  The  exciting  and  fostering  causes  are  often 
mental  and  nervous  strain.  While  the  symptoms  of  the  disease,  the 
nervousness,  the  insomnia,  and  the  vasomotor  disturbances  are  due  to  the 
hypersecretion  of  thyroid,  the  morbid  disturbance  often  may  well  be 
fundamentally  a  loss  of  central  nervous  control.  If  the  nervous  centres 
can  be  kept  quiet  long  enough,  the  demand  on  their  part  for  this  excess 
of  thyroid  juice  gradually  ceases  and  the  patient  gets  well.  This  is  the 
rationale  of  the  prolonged  rest  which  is  the  real  and  specific  cure  for 
the  disease  in  its  ordinary  phases. 


558  DISEASES    OF    THE    NERVOUS    SYSTEM 

Prognosis. — About  one-fifth  of  the  cases  get  well  or  practically  well. 
Probably  over  half  the  cases,  if  they  can  be  properly  treated,  reach  a 
fairly  comfortable  condition  of  improvement.  The  cases  in  which 
symptoms  come  on  quickly  have  the  most  favorable  prognosis.  In 
those  with  marked  exophthalmus  and  goitre  the  prognosis  is  not  so 
good.  The  duration  of  the  disease  in  recovering  cases  is  from  two  to 
eight  years.  A  later  development  of  hypo-thyroidism  and  myxoedema 
is  not  in  accord  with  my  observation  though  it  may  occur.  I  have 
recently  seen  three  now  healthy  patients  who  had  Graves'  disease  over 
twenty  years  ago. 

Diagnosis. — The  disease  can  be  distinguished  by  the  persistent 
tachycardia,  with  goitre  or  exophthalmus,  and  in  its  early  stage  by 
the  tachycardia  with  tremor,  moist  skin,  sensations  of  heat,  nervous- 
ness, emaciation,  insomnia,  lessened  respiratory  expansion,  and  electrical 
resistance. 

A  symptomatic  Graves'  disease  may  sometimes  be  caused  by  a 
goitre  pressing  on  the  vagus  or  sympathetic  and  causing  irregular  heart 
beat  and  perhaps  exophthalmus.  In  these  cases  the  history  of  a  long- 
standing goitre  exists,  the  heart's  action  is  irregular,  the  exophthalmus 
is  usually  partial  and  one-sided.  In  abortive  forms  it  is  necessary 
to  have  tachycardia  and  at  least  one  other  of  the  four  major  symptoms 
to  make  a  diagnosis  of  Graves  disease. 

Treatment. — Rest  is  the  most  important  single  thing.  The  patients 
sometimes  need  to  be  put  to  bed  or  kept  on  the  back  for  one  to  three 
months.  Sometimes  a  half-rest  is  enough,  with  freedom  from  excite- 
ment and  worry,  A  sea  voyage  can  be  worked  in  with  advantage.  No 
special  diet  is  needed,  nor  do  climatic  influences  or  baths  or  mineral 
waters  have  much  effect,  except  in  so  far  as  they  secure  a  quieter  and 
better  environment. 

The  drugs  used  are  numerous.  Of  these,  the  phosphates,  the  lime 
salts,  iodine,  strophanthus,  aconite,  belladonna,  bromides,  and  iron  have 
served  best.  In  certain  very  mild  cases  with  small  goitres,  thyroid 
extract  in  small  doses  does  good,  but  as  a  rule  it  is  harmful. 

Beebe  and  Rogers  have  obtained  an  anti-thyroid  serum  which,  in 
acute  and  serious  cases  where  there  is  great  thyroid  toxaemia,  acts  suc- 
cessfully. In  the  more  chronic  and  quiescent  cases  it  is  not  so  efficient. 
Beebe  has  recently  prepared  another  serum  which  is  given  hypodermic- 
ally.     A  serum  from  thyroiclectomized  goats  has  given  some  results. 

The  surgical  treatment  of  exophthalmic  goitre  is  not  always  successful; 
and  it  sometimes  happens  that  symptoms  of  hypothyroidism  develop  later. 
It  is  best  to  get  the  patient  into  a  relatively  quiescent  state  by  medical 
treatment  and  rest  before  operating.  And  it  is  advisable  usually  to  begin 
with  ligation  of  arteries  in  order  to  see  whether  this  may  not  be  sufficient 


EXOPHTHALMIC    GOITRE  559 

before  any  of  the  gland  is  removed.  According  to  Rogers  the  ligation 
under  local  anaesthesia  of  one  or  more  of  the  thyroid  vessels  or  the  removal 
of  one-half  or  more  of  the  thyroid  gland  yields  about  50  per  cent,  of 
cures.  Ligature  of  the  arteries  is  safer  but  not  so  immediately  efficient 
as  thyroidectomy.  If  the  patient  needs  for  economic  reasons  prompt 
relief,  with  a  certain  attendant  risk,  he  should  try  surgery,  at  least  till 
we  have  better  medical  measures  than  we  have  at  present.  Surgery,  or 
at  least  thyroidectomy,  is  dangerous  in  actively  progressive  cases  and  in 
those  associated  with  a  psychosis.^ 

The  X-ray  and  radium  are  said  to  have  value,  and  I  have  seen  the 
latter  accomplish  results. 

For  the  palpitations,  the  ice  bag  placed  over  the  heart  and  neck  is 
helpful  and  may  be  used  systematically. 

1  S.  Landstrom's  statistics  of  cases  of  himself,  Kocher,  Mayo,  Riedel  gave  cure  or 
improvement  in  about  80  per  cent. ;  death  in  about  10  per  cent.  Landstrom  in  38 
cases  reports  cure  in  48.7  per  cent.,  improvement  in  17.1  per  cent.,  failure  in  26.8 
per  cent.,  death  in  7.4  per  cent.  Mayo's  figures  on  cures  or  improvement  87.8  per 
cent.,  death,  12.2  per  cent. 


CHAPTER  XXVI 
PROFESSIONAL  NEUROSES,  OCCUPATION  NEUROSES 

(Writer's  Cramp  and  Allied  Affections) 

Writer's  cramp  is  a  nervous  affection  characterized  by  spasmodic, 
tremulous,  or  paralytic  disturbances,  occurring  when  the  act  of  writing 
is  attempted.  Since  the  introduction  of  the  typewriter,  writer's  cramp 
has  become  less  common.  In  its  place  we  have,  with  relative  less  fre- 
quency, stenographer's  and  typewriter's  cramps. 

Etiology. — It  is  a  disease  of  modern  times,  and  has  been  particularly 
noted  since  the  introduction  of  steel  pens,  about  the  year  1820.  A 
neuropathic  constitution  is  often  present,  and  sometimes  there  is  a 
hereditary  history.  Men  are  much  more  subject  to  the  disease  than 
women.  The  most  susceptible  age  is  between  twenty-five  and  forty. 
It  rarel}^  occurs  after  fifty  or  before  twenty.  Clerks  and  professional 
writers  are  naturally  much  more  subject  to  the  disease.  Excessive  worry, 
intemperance,  and  all  debilitating  influences  predispose  to  it.  The  chief 
exciting  cause  is  excessive  writing.  But  this  is  not  all.  The  writing 
that  is  done  under  strain  or  a  desire  to  finish  a  set  task  is  the  harmful 
thing.  The  style  of  writing  is  also  an  important  factor.  Writing 
done  in  a  cramped  posture  with  movements  of  the  finger  alone  or  with 
the  little  finger  or  wrist  resting  on  the  table  is  most  injurious.  Free- 
hand writing  done  from  the  shoulder  according  to  the  American  system 
is  least  harmful.  Shaded  or  heavy  writing  with  sharp  steel  pens  is  also 
productive  of  harm.  Copying  is  much  more  harmful  than  composing. 
Authors  seldom  have  writer's  cramp.  The  performance  under  strain 
of  some  specially  prolonged  task  is  the  most  common  exciting  cause. 
Injury  and  exposure  to  wet  and  cold  occasionally  start  the  trouble. 

Symptoms. — Writer's  cramp  very  rarely  attacks  a  person  suddenly. 
The  patient  first  notices  a  certain  amount  of  stiffness  occurring  at 
times  in  the  fingers,  or  the  pen  is  carried  with  some  uncertainty  and 
jerky  movements  are  made.  He  feels  a  sensation  of  fatigue  in  the 
hand  and  arm,  and  this  may  amount  to  an  actual  tired  pain.  The 
first  symptoms  may  last  for  months  or  even  years.  The  hand  is  rested 
as  much  as  possible;  new  pens  or  penholders  and  new  modes  of  holding 
it  are  tried.  Often  the  patient,  fearing  the  onset  of  the  cramp,  and  as 
its  result  loss  of  employment,  becomes  anxious,  worried,  and  mentally 

560 


PROFESSIONAL    NEUROSES,    OCCUPATION    NEUROSES  561 

depressed.  Sometimes  the  trouble  is  worse  when  beginning  a  daily 
task,  and  it  gradually  wears  off  in  a  few  hours.  At  other  times  exactly 
the  reverse  is  the  case.  When  the  disease  has  reached  its  highest  stage, 
writing  becomes  almost  or  entirely  impossible.  The  moment  the  pen 
is  taken  in  the  hand  and  an  attempt  at  using  it  made,  spasmodic 
contractions  of  some  of  the  fingers,  or  even  of  the  arm,  occur,  the  pen 
flies  in  any  direction,  and  it  is  impossible  to  control  or  co-ordinate  the 
movements.  The  rule  is  that,  although  writing  cannot  be  done,  all 
other  complex  movements  are  performed  as  well  as  ever.  Thus  the 
sufferer  from  writer's  cramp  may  be  able  to  play  the  piano,  or  paint,  or 
thread  a  needle,  or  use  the  hand  in  any  complex  movements.  This 
limitation,  however,  is  not  always  present.  Telegraphers,  who  use  to 
some  extent  the  same  muscles  as  in  writing,  and  who  also  often  have  to 
do  a  great  deal  of  writing,  are  liable  to  suffer  from  both  writer's  and 
telegrapher's  cramp  at  the  same  time.  No  evidences  of  actual  paralysis 
are  present  in  the  affected  muscles  and  there  is  rarely  anaesthesia,  but 
the  arm  aches  and  is  sometimes  tender.  Sensations  of  numbness  and 
prickling  are  present  and  occasionally  a  complicating  neuritis  develops. 
In  rare  cases  vasomotor  disturbances  are  observed.  There  are  sometimes 
associated  muscular  movements  of  the  other  arm  or  of  the  neck. 

The  various  symptoms  occur  with  different  degrees  of  prominence, 
so  that  the  disease  has  been  classed  under  the  heads  of  (1)  the  spastic, 
(2)  the  neuralgic  or  sensory,  (3)  the  tremulous,  and  (4)  the  paralytic 
forms.     These  forms  are,  however,  often  more  or  less  mixed. 

1.  The  spastic  form  is  undoubtedly  the  most  common,  and  it  has 
given  to  the  disease  its  name.  Cramp  of  some  muscle  or  muscles  is 
present  in  over  half  of  the  cases.  The  muscles  of  the  thumb  and  first 
three  fingers  are  oftenest  affected,  and  in  some  cases  the  flexors,  in  some 
the  extensors,  are  chiefly  involved.  In  telegrapher's  cramp  it  is  the 
extensors,  but  in  writer's  cramp  the  flexors,  that  are  mainly  attacked. 

2.  The  neuralgic  form  resembles  the  spastic  plus  sensations  of 
fatigue  and  pain,  which  are  quite  severe  and  are  brought  on  by  writing. 
There  may  be  tenderness  over  the  arm  nerves  also. 

3.  The  tremulous  type,  though  rare,  is  very  characteristic.  The 
patient  when  attempting  to  write  develops  a  tremulous  movement 
of  his  hand  and  arm.  This  ceases  when  his  attempts  to  write  cease. 
The  tremor  usually  affects  most  the  fingers  used  in  pen  prehension,  but 
it  also  spreads  to  the  forearm  and  may  even  involve  the  entire  extremity. 
Although  this  tremor  develops  on  attempting  to  write,  it  does  not  de- 
velop on  other  voluntary  movements. 

4.  The  paralytic  form,  or  that  type  in  which  muscular  feebleness 
is  the  dominant  symptom,  is  also  rare.  In  the  typical  paralytic  form  the 
patient,  as  soon  as  he  begins  to  write,  feels  an  overpowering  sense  of  weak- 

36 


562  DISEASES    OF    THE    NERVOUS    SYSTEM 

ness  and  fatigue  in  the  fingers  and  arm.     The  fingers  themselves  loosen 
their  grip  and  the  pen  may  drop  from  the  hand. 

Associated  Symptoms. — Writer's  cramp  is  essentially  a  motor  neurosis, 
and  its  leading  symptom  is  the  impairment  of  a  motor  function.  Other 
symptoms,  however,  both  general  and  local,  are  always  associated  with 
it.  These  are  mainly  (1)  psychical  and  (2)  sensory,  more  rarely  (3) 
vasomotor  and  (4)  trophic. 

1.  Psychical  Symptoms. — -The  patient  is  often  nervous,  emotional, 
and  mentally  depressed  at  times.  He  suffers  from  insomnia  and  vertigo. 
Patients  are  generally  unwilling  to  admit  that  there  is  any  other  trouble 
than  the  local  one,  and  only  careful  examination  may  bring  evidence  of 
constitutional  trouble.  There  are  cases  of  purely  mental  writer's 
cramp. 

2.  Sensory  Troubles. — ^These  consist  of  pains,  sense  of  fatigue,  feel- 
ings of  numbness,  prickling,  pressure,  weight,  tension,  constriction, 
etc.  Hyperesthesia  and,  more  rarely,  anaesthesia  are  also  observed. 
The  most  common  sensory  symptom  is  that  of  aching  and  fatigue,  and 
this  is  usually  confined  to  the  arm,  and  oftenest  runs  along  the  course 
of  the  rachal  and  median  nerves.  The  cervical  vertebrae  may  be  tender 
and  sometimes  patients  have  a  headache  in  the  parietal  region  of  the 
side  opposite  the  affected  arm. 

3.  Vasomotor,  Trophic,  and  Secretory  Disturbances. — ^The  condition 
known  as  digiti  mortui  has  been  observed,  coming  on  paroxysmally. 
In  acute  cases  of  writer's  cramp  with  associated  neuritis  decided  vascular 
changes  may  occur,  such  as  passive  congestion  of  the  hand  and  arm, 
with  swelling  and  turgescence  of  the  fingers,  and  a  sensation  of  throbbing. 
In  bad  cases  the  fingers  will  look  as  if  they  had  chilblains. 

Electrical  Reactions. — Ordinary  tests  will,  as  a  rule,  reveal  very  little 
change.  Sometimes  there  is  a  quantitative  increase,  sometimes  a 
decrease,  of  irritability  to  both  forms  of  current. 

Pathology. — Neuritis  is  undoubtedly  present  in  some  forms  of 
writer's  cramp,  so  called.  It  is  not  present,  however,  so  far  as  external 
tests  go,  m  the  typical  neurosis.  Nor  are  there  any  post-mortem  ob- 
servations throwing  light  on  the  anatomy  of  the  disease.  We  must  believe, 
therefore,  that  it  is  a  neurosis  having  no  appreciable  anatomical  basis. 

While  writer's  cramp  is  often  complicated  with  some  neuritic  dis- 
turbance leading  to  symptoms  in  the  affected  arm  of  pain,  paralysis, 
tenderness  over  nerves,  vasomotor  disturbances,  etc.,  there  can  be  no 
doubt  that  the  lesion  in  typical  cases  is  central  and  involves  the  higher 
reflex  centres  and  indirect  motor  and  sensory  paths.  Little  more 
can  be  said  of  the  pathology  than  that  it  is  an  "exhaustion  neurosis," 
and  that  its  mechanism  is  allied  to  the  spasmodic  tics  and  especially  to 
stuttering.     The  same  is  true  of  all  the  other    forms    of    occupation 


PKOFESSIONAL    NEUROSES,    OCCUPATION    NEUROSES  563 

neuroses,  and  nothing  need  be  said  upon  this  point  regarding  them 
when  they  come  to  be  considered. 

The  diagnosis  of  well-marked  cases  of  writer's  cramp  presents  no 
difficulty.  In  the  earlier  stages,  however,  it  may  be  confounded  with 
a  large  number  of  disorders,  viz.,  post-hemiplegic  chorea,  hemiataxia, 
paralysis  agitans,  progressive  muscular  atrophy,  progressive  locomotor 
ataxia,  various  forms  of  tremor,  lead  paralysis,  rheumatoid  arthritis, 
neuritis,  cerebral  and  nerve  tumors,  and  tenosynovitis. 

In  many  of  these  cases  it  is  only  necessary  to  bear  in  mind  the  history 
of  the  disease  in  order  at  once  to  reach  a  safe  conclusion  as  to  its  nature. 

If  there  is  a  great  deal  of  pain  in  the  arm,  with  tenderness  along 
the  course  of  the  nerves;  if  there  is  decided  change  in  the  electrical 
reactions;  if  there  are  sensations  of  tingling,  numbness,  etc.;  and  if 
the  patient  shows  an  absolute  loss  of  power  in  the  various  groups  of 
muscles,  with  some  incapacity  for  doing  other  acts  besides  the  one 
with  which  he  is  specially  concerned,  then  the  trouble  is  undoubtedly 
peripheral  and  due  largely  to  an  underlying  neuritis.  The  prognosis 
in  these  cases  is  much  more  favorable.  If,  on  the  other  hand,  the  dis- 
order comes  on  in  persons  who  have  done  an  excessive  amount  of  writing; 
if  it  is  associated  with  nerve  strain;  if  the  electrical  reactions  are  but 
slightly  changed,  the  sensory  symptoms  slight  and  the  motor  inco- 
ordination is  marked,  limited  to  the  special  class  of  work,  and  not  ac- 
companied with  absolute  paresis,  the  disorder  is  central  and  needs  both 
a  different  treatment  and  prognosis. 

Course  and  Duration. — Writers'  cramp  is  a  chronic  disease.  It 
begins  insidiously  and  attacks  one  group  of  muscles  after  another  as 
each  is  brought  into  play  by  new  methods  of  writing.  If  the  left  hand 
is  used,  that,  too,  is  liable  to  become  affected.  The  course  varies,  how- 
ever; for  a  time  progress  may  be  arrested  or  improvement  set  in.  When 
the  disease  becomes  well  established  it  will  most  often  last  a  lifetime. 

Prognosis. — -The  prognosis  is  unfavorable,  yet  not  so  much  so  as 
was  once  thought.  Undoubted  cases  of  complete  recovery  have  been 
reported,  even  under  unfavorable  conditions.  The  prognosis  is  much 
more  favorable  if  the  patient  begins  treatment  early  and  before  marked 
spastic  symptoms  are  present.  It  is  more  favorable  in  the  neuralgic 
forms.  Some  patients  who  suffer  from  a  mild  form  of  the  trouble  manage, 
by  the  help  of  instruments  or  special  pens,  to  do  their  work  for  years. 
The  more  acute  the  disease  and  the  more  evidently  peripheral  and 
neuritic  its  origin,  the  better  the  prognosis.  In  over  one-fourth  of  the 
cases,  patients  who  use  their  sound  arm  will  not  be  affected  in  it. 

The  facts  stated  regarding  the  cause,  physiology,  and  general  symp- 
tomatology of  writers'  cramp  apply  to  the  other  forms  of  occupation 
neuroses.     A  few  special  details,  however,  will  be  given  regarding  these. 


564  DISEASES    OF    THE    NERVOUS    SYSTEM 

The  most  common  and  important  are  musicians'  cramp  and  telegraphers' 
cramp. 

Musicians'  Cramp. — Under  this  head  we  include  pianists'  cramp,  vioKnists'  cramp, 
flutists'  cramp,  and  the  cranip  of  clarionet  players. 

Pianists'  cramp  occurs  usually  in  young  women  who  are  studying  to  become  pro- 
fessionals or  who  are  especially  hard  working  and  ambitious.  The  absurd  "Stuttgart 
method"  of  teaching  the  piano,  in  which  the  motions  are  confined  as  much  as  possible 
to  the  fingers,  predisposes  especiallj^  to  this  disease.  The  symptoms  are  those  of 
fatigue,  pain,  and  weakness.  The  pains  are  of  an  aching  character.  They  are  felt 
in  the  forearm  especially,  but  extend  up  the  arm  and  between  the  shoulders.  Spas- 
modic symptoms  are  rare.  The  right  hand  is  oftener  affected,  but  both  hands  even- 
tually become  involved. 

Violinists'  cramp  may  attack  the  right  hand  which  holds  the  bow  or  the  left  hand 
which  fingers  the  strings,  but  more  often  the  left  hand  is  affected. 

Clarionet  players  sometimes  suffer  from  cramp  of  the  tongue  and  of  the  laryngeal 
muscles. 

Flute  players  suffer  not  very  infrequently  from  slight  laryngeal  spasms.  A  similar 
trouble  affects  elocutionists.     The  term  mogophonia  is  applied  to  this  type. 

Telegraphers'  cramp  affects  especially  those  operators  using  the  Morse  system,  which 
is  still  the  one  most  widely  in  vogue.  Contrary  to  the  opinions  of  previous  writers, 
Dr.  Lewis  believes  that  this  neurosis  is  not  a  rare  one  and  is  destined  to  become  more 
frequent.  In  this  city  the  cramp  is  not  rare,  the  proportion  being  about  one  in  every 
two  hundred.  The  technical  name  among  operators  for  the  cramp  is  "loss  of  the 
grip."  In  telegraphing,  the  extensors  of  the  wrist  and  fingers  are  called  most  into 
play,  and  hence  are  most  and  earliest  affected.  The  symptoms  come  on  very  slowly, 
the  thumb  and  index-finger  being  first  affected.  The  victim  finds  that  he  cannot  de- 
press the  key  on  account  of  spasm  in  these  muscles,  and  he  finds  most  difficulty  in 

making  the  dot  characters,  such  as  h  (....),  or  p  ( ),  or  z  (.  .  .    .).     When  the 

flexors  are  most  affected,  the  key  is  depressed  with  undue  force  and  a  dash  is  made 
instead  of  a  dot.  Sufferers  from  the  "loss  of  grip"  generally  have  writers'  cramp  also. 
While  spasm  is  usually  present,  the  disease  may  show  itself  simply  in  pain,  paresis, 
and  incapacity  to  co-ordinate  the  muscles. 

In  sewing-spasm,  which  affects  tailors,  seamstresses,  and  shoemakers,  clonic  and 
tonic  spasms  attack  the  muscles  of  the  hands  on  attempting  to  use  them  in  the  regular 
work.  Tailors  who  sit  crosslegged  sometimes  suffer  from  a  peculiar  spasm  on  assum- 
ing this  position. 

Smiths'  spasm,  or  "hephcestic  hemiplegia"  appears  to  have  been  observed  only  by 
Duchenne  and  Dr.  Frank  Smith.  It  occurs  in  persons  engaged  in  pen-blade  manu- 
facturing, saw  straightening,  razor-blade  striking,  scissors  making,  file  forging,  etc. 
In  doing  this  work  they  have  to  use  a  light  or  heavy  hammer,  with  which  strokes  are 
delivered  very  rajDidly  and  carefully.  After  a  time  spasmodic  movements  occur  in 
the  arm  used,  and  the  arm  falls  powerless.  As  in  the  cases  reported,  there  are  gen- 
erally hemiplegic  symptoms,  and  also  neuralgias,  vertigo,  and  other  cerebral  troubles, 
the  disease  cannot  be  a  purely  functional  neurosis. 

Drivers'  spasm  has  been  observed  in  veterinary  surgeons  by  Dr.  Samuel  Wilkes. 

Milkers'  spasm  is  an  extremely  rare  affection,  which  was  first  described  by  Basedow 
and  seems  to  occur  in  milkmaids,  never  in  milkmen. 

Cigarmakers'  cramp  is  very  rare  and  often  associated  with  some  neuritis. 

Watchmakers'  cra?np  and  photographers'  cramp  are  also  to  be  regarded  merely  as 
pathological  curiosities. 


PROFESSIONAL    NEUROSES,    OCCUPATION    NEUROSES 


565 


Ballet- Dancers'  cramp. — Under  this  name  certain  painful  and  parah'tic  troubles 
occurring  in  ballet  dancers,  especially  j^remieres  danseuses,  have  been  described  by 
Schultz,  Onimus,  and  Kraussold.  It  does  not  appear  that  the  trouble  is  really  a  co- 
ordinative  functional  one,  but  is  rather  neuralgic  or  the  result  of  local  strain  upon  the 
parts. 

The  list  of  professional  neuroses  is  made  to  include,  besides  those  above  given, 
cramps  and  co-ordinative  troubles  affecting  artificial-flower  makers,  billiard  players^ 
dentists,  hide  dressers,  drummers,  electrical  instrument  makers,  stampers,  turners, 
sewing-machine  girls,  money  counters,  weavers,  painters  and  pedestrians. 

Prophylaxis  and  Treatment. — The  introduction  of  typewriters, 
gold  pens,  and  improved  penholders  has  prevented  somewhat  the  in- 
crease of  writers'  cramp.  Stenographers  rarely  have  it  unless  they  write 
in  long  hand  also.  Persons  who  have  to  write  a  great  deal  should  use 
large  cork  or  rubber  penholders  and  gold  or  quill  pens  with  smooth 
paper.     The  best  style  of  writing  is  that  done  from  the  shoulder,  but 


Fig.  239. — Mathieu's  instrument 
for  writers'  cramp. 


Fig.  240. — JN'ussbaum's  instrument. 


this  is  a  method  that  bookkeepers  and  those  who  have  to  keep  accounts 
cannot  easily  adopt.  Many  nervous  persons  have  a  bad  habit  of  gripping 
the  pen  very  tightly  and  pressing  down  on  the  paper  with  excessive  force. 
Fatigue  soon  results  and  painful  sensations  develop  in  the  arm.  Proper 
attention  should  be  paid  to  the  position  of  the  paper  written  upon,  the 
height  of  the  desk,  the  light,  and  the  sleeves  of  the  coat  or  dress.  The 
paper  should  be  laid  at  an  oblique  angle  to  the  edge  of  the  desk,  and 
not  at  a  right  angle  as  many  writing-teachers  are  accustomed  to  direct. 
As  some  cases  of  "cramp"  are  undoubtedly  cerebral,  it  is  very  unwise 
to  attempt  any  extraordinary  exploits  in  writing  or  to  work  with  the 
ambition  to  put  the  writing-capacity  to  the  utmost  test. 

When  the  cramp  is  fully  developed,  the  most  essential  thing  is 
rest,  and  it  is  generally  best  to  advise  the  patient  to  change  his  occupa- 
tion at  once.  Some  rest,  however,  may  be  secured  by  getting  a  new 
form  of  penholder,  holding  the  pen  in  a  different  way,  using  the  unaffected 
arm,  or  using   some   form  of   mechanical   appliance.     The   mechanical 


566  DISEASES    OF    THE    NERVOUS    SYSTEM 

appliances  are  splints,  rubber  bands  around  the  wrist,  and  various  in- 
struments contrived  to  prevent  spasm  and  throw  the  work  of  writing  on 
new  and  larger  groups  of  muscles. 

Instruments  for  writers'  cramp  are  very  numerous.  Those  that  are 
of  some  value  are  Mathieu's,  Nussbaum's,  and  some  modification  of 
Cazenave's  (see  Figs.  239,  240).  All  the  various  instruments  have 
been  of  service,  or  have  even  been  curative  in  some  special  cases,  but 
not  too  much  must  be  expected  of  them.  As  a  rule,  they  are  only  pallia- 
tive.    A  cheap  instrument  that  may  prove  satisfactory  is  that  of  Mathieu. 

In  the  medical  treatment  of  writers'  cramp  the  important  agents 
are  massage,  pedagogics,  and  rest. 


CHAPTER  XXVII 
PARALYSIS  AGITANS 

(Shaking  Palsy,  Parkinson's  Disease) 

Paralysis  agitans  is  a  chronic  progressive  disease,  characterized 
by  tremor,  muscular  rigidity  and  weakness,  and  by  a  peculiar  attitude 
and  gait,  together  with  sensations  of  heat,  pain,  and  restlessness. 

Etiology. — -The  disease  occurs  more  often  among  men  than  women 
in  the  proportion  almost  exactly  of  2  to  1  (155  males,  82  females).  More 
than  two-thirds  of  the  cases  occur  between  the  ages  of  45  and  60,  and 
the  serious  decade  is  the  fifth.  Practically  no  cases  occur  before  35 
and  very  few  before  40. 

In  127  personal  cases  the  age  of  development  of  the  disease  was: 


20-30, 

2 

30-40, 

8 

40-50, 

40 

50-60, 

46 

60-70, 

24 

70-80, 

7 

127 

The  disease  is  by  no  means  rare  in  this  country  and  affects  the 
native  stock  seriously.  Among  90  private  cases  47  were  of  distinctly 
American  stock,  13  occurred  among  Hebrews,  and  8  among  Germans,  8 
among  Irish.  It  is  not  especially  an  urban  disease,  many  cases  coming 
from  small  towns.  It  affects  educated  and  professional  classes  more 
than  it  does  laboring  men.  Fifteen  per  cent,  of  my  private  cases  were 
lawyers,  doctors  and  clergymen,  one  was  an  engineer  and  one  a  teacher. 
It  is  a  disease  of  brain-workers  more  than  muscle-workers. 

Hereditary  influence  has  some  importance.  Among  90  cases  there 
was  a  history  of  apoplexy,  heart  or  renal  cUsease  in  the  direct  ascendants 
in  19  cases,  showing  a  weakness  in  the  direction  of  the  circulatory  sys- 
tem. There  was  a  direct  heredity  of  paralysis  agitans  in  2,  an  in- 
direct (paternal  uncle  and  aunt)  in  2,  and  a  family  or  senile  tremor 
among  8.  Thus  about  15  per  cent,  show  a  hereditary  weakness  as 
regards  tremor.  Melancholia  was  present  in  the  ascendants  of  7  cases, 
and  a  tendency  to  anxious  depression  is  very  common  among  the  patients 

567 


568 


DISEASES    OF    THE    NERVOUS    SYSTEM 


themselves,  three  of  whom  had  the  melancholia  of  involution.  Dia- 
betes was  present  in  the  ascendants  in  2  cases  and  in  3  of  the  patients 
themselves.     Not  many  families,   aside  from  those  referred  to,   were 

neurotic  or  rheumatic,  and  the 
children  of  the  patients  were  al- 
most uniformly  reported  healthy. 
Some  hereditary  influence  thus  is 
present  in  10  to  20  per  cent.,  shown 
mainly  in  a  tendency  to  benign 
tremor,  stuttering  or  a  tic,  or  in 
arterial  sclerosis  leading  to  cardiac 
cUsease  and  cerebral  hemorrhage. 
Paralysis  agitans  is  distinctly  a 
disease  of  sober  living.  It  is  not 
caused  by  the  ordinary  departures 
from  lectitude,  such  as  dissipation, 
sexual,  alcoholic,  tobacco  or  food 
excess  or  even  by  lues.  The  thing 
most  commonly  observed  is  a  regu- 
lar laborious  and  anxious  life.  The 
patient,  if  a  man,  has  not  been  a 
vacation  man,  and  his  habits  have 
been,  if  anything,  abnormally  regu- 
lar. Among  direct  causes,  there 
can  be  no  doubt  that  work  and 
worry  and  psychic  trauma  are  the 
most  important. 

Shock  and  injury  are  noted  in 
2  per  cent,  of  cases,  but  the  influ- 
ence is  not  important  in  all  of 
them.  In  the  working  classes,  ex- 
posure and  hard  work  are  cited  as 
causes,  but  there  is  usually  a  men- 
tal element  of  anxiety  also.  About 
10  per  cent,  of  men  are  smokers, 
very  few  (4  per  cent.)  are  drinkers, 
and  syphilis  is  almost  never  present 
(2  cases). 
Rheumatism  has  been  put  down  as  a  cause,  but  few  patients  are 
really  sufferers  from  articular  rheumatism.  Many,  however,  as  the 
disease  comes  on,  suffer  from  lumbago,  sciatica  and  various  forms  of 
muscular  pain,  which  are  usually  rather  premonitions  than  causes  of 
the  disease. 


Fig.  241.— The  attitude  in  paralysis  agitans. 


PAEALYSIS    AGITANS  569 

Diabetes  was  present  in  three  cases,  but  it  is  probably  a  coincidence. 

It  sometimes  follows  acute  infections  and  has  perhaps  a  relationship 
to  rheumatoid  arthritis,  or  metabolic  and  autotoxic  rheumatic  condi- 
tions. The  view  that  it  is  a  "parainfectious"  malady,  due  to  the  late 
action  of  an  infection,  has  been  suggested. 

Symptoms. — The  disease  is  sometimes  ushered  in  with  an  acute 
illness,  or  an  attack  of  neuralgia.  It  usually  develops  slowly  with  some 
aching  pains  in  the  arm  and  a  slight  tremor  in  the  fingers  of  one  hand, 
oftener  the  right.  For  a  period  of  several  months  the  patient  perhaps 
simply  knows  that  he  has  an  arm.  Then  the  tremor  becomes  distinctly 
marked  in  the  hand.  It  gradually  extends  and  involves  the  leg  of 
the  same  side,  then  the  other  side  becomes  affected.  The  neck,  face, 
and  tongue  are  rarely  attacked  by  tremor,  and  then  to  a  small 
extent.  After  or  with  the  tremor  there  comes  on  a  stiffness  in  the  arms 
and  legs,  and  indeed  of  the  whole  body.  With  this  there  is  a  general 
contracturing  and  shortening  of  all  the  flexor  groups,  so  that  the  head 
and  body  are  bent  forward,  the  fingers  are  straight  but  are  flexed  as  a 
whole  on  the  metacarpus,  the  forearms  flexed  on  the  arm,  the  trunk  is 
flexed  forward  on  the  thighs,  and  the  knees  are  slightly  bent.  The 
attitude  gives  the  idea  of  extreme  senility  (Fig.  241).  The  gait  is  slow, 
the  steps  are  short  and  shuffling;  the  patient  has  trouble  in  starting, 
stopping,  and  turning  corners,  owing  to  the  slowness  in  initiating  new 
movements  in  the  voluntary  muscles.  When  once  started,  he  may  be 
unable  to  stop  and  has  to  run  along.  The  speech  becomes  affected  in 
one  or  two  years.  The  voice  is  high-pitched,  weak,  and  piping,  or 
senile  in  quality.  There  is  a  slowness  in  getting  out  words  or  in  start- 
ing a  sentence,  though  after  it  is  begun  the  words  come  rapidly.  The 
condition  is  analogous  to  the  festination  in  the  gait. 

Along  with  the  other  symptoms,  there  are  often,  though  not  always, 
sensations  of  heat,  burning,  fever,  and  rarely  of  coldness.  These  sen- 
sations are  felt  most  in  the  feet,  legs,  or  arms  diffusely.  Often  there  is 
a  general  feeling  of  restlessness  and  nervousness.  Aching  pains  and  a 
sense  of  fatigue  occur;  neuralgic  pains  are  more  rare.  There  are  al- 
ways a  peculiar  redness  and  flush  in  the  faces  of  the  patients.  Some- 
times they  sweat  profusely.  The  temperature  in  the  axilla  is  normal, 
on  the  skin  it  is  sometimes  increased.  The  appetite  is  excellent,  often 
abnormafly  great,  and  digestion  is  good.  Visceral  complications  are 
rare.  Muscular  weakness  comes  on  early;  it  slowly  increases,  but  real 
muscular  paralysis  does  not  occur.  The  disease  ends  in  rigidity,  which 
makes  the  patient  as  helpless  as  if  paralyzed,  but  the  muscles  pre- 
serve considerable  functional  power  to  the  last.  The  deep  reflexes 
are  present  and  not,  as  a  rule,  exaggerated;  but  exaggeration  and  even 
clonus  occur  in  a  small  percentage  of  cases.     As  the  disease  progresses 


570  DISEASES    OF    THE    NERVOUS    SYSTEM 

the  tremor  increases  in  extent,  and  continues  with  little  remission  dur- 
ing all  the  waking  hours;  later  the  limbs  get  more  rigid  and  in  a  way 
this  rigidity  drowns  out  the  tremor;  the  patient  becomes  weaker  and 
suffers  keenly  from  sensations  of  fatigue  and  exhaustion.  At  last  he 
can  no  longer  walk;  he  becomes  bedridden  and  is  finally  carried  off  by 
exhaustion  or  some  intercurrent  illness. 

It  will  be  seen  that  the  dominant  symptoms  in  paralysis  agitans  are: 

1.  Tremor. 

2.  Rigidity,    progressively   increasing,    with   trunk   deformities   and 
contractures. 

3.  Muscular  weakness. 

4.  Sensory,  vasomotor  and  metabolic  disturbances. 
Further  details  must  be  given  regarding  these  symptoms: 


Fig.  242. — Festination  in  paralysis  agitans. 

The  tremor  is  a  coarse  one.  It  ranges  from  about  6  vibrations  per 
second  to  3.7.  The  average  rapidity  is  4  or  5  per  second,  which  is  about 
one-half  the  normal  muscular  rhythm.  But  the  chief  characteristic 
of  the  tremor  is  that  it  continues  when  the  hand  or  limb  is  at  rest,  while 
voluntary  motion  causes  it  to  cease.  As  the  hand  rests  on  the  knee 
it  shakes;  as  it  is  moved  the  tremor  stops.  When  held  straight  out 
there  is  no  shaking  for  a  moment,  but  it  soon  begins.  A  glass  of  water 
is  carried  safely  to  the  lips.  The  patient  can  control  the  tremor  for 
a  moment,  especially  in  the  early  stages  of  the  disease.  These  facts 
about  the  tremor  apply  in  90  per  cent,  of  cases,  but  there  are  patients 
whose  tremor  is  slight  when  the  limb  is  at  rest  and  is  increased  on  volun- 
tary effort.  The  hands  are  affected  in  a  characteristic  way.  The  fingers 
and  thumb  are  slightly  flexed  and  held  about  in  the  writing-position; 
the  tremor  moves  the  fingers  and  thumb  as  a  whole,  and  they  vibrate 


PARALYSIS    AGITANS  571 

SO  that  the  one  pats  the  other  gently.  Sometimes  the  tremor  is  one  of 
alternate  supination  and  pronation  of  the  forearm.  The  neck  and  face 
muscles  are  not  usually  or  extensively  involved,  the  shaking  of  the  head 
being  generally  the  result  of  the  general  bodily  tremor.  Sometimes  one 
sees  a  tremor  of  the  lips  or  neck  muscles.  The  tongue  and  eye  muscles 
are  practically  never  involved  in  tremor. 

Rigidity. — The  rigidity  comes  on  early,  and  may  be  the  first  and 
even  the  only  prominent  symptom.  It  affects  chiefly  the  flexors  of  the 
arms,  head  and  trunk,  and  legs,  producing  a  characteristic  senile  posi- 
tion. In  rare  cases  the  extensors  of  the  neck  are  affected  and  the  head 
is  drawn  back.  Cramps  occur,  and  there  is  always  a  sense  of  stiffness. 
The  muscular  movements  are  slow,  especially  the  initiation  of  a  move- 
ment. Once  started,  a  motion  may  be  quickly  done.  The  gait  is 
peculiar;  the  steps  are  short  and  shuffling;  the  patient  may  have  dif- 
ficulty in  starting;  but  once  started  he  goes  very  well;  or  while  walk- 
ing there  may  be  a  sudden  running  forward.  This  is  called  "festi- 
nation."  Rarely  there  is  a  tendency  to  run  backward  or  sideways. 
Some  muscular  weakness  sets  in  early  and  slowly  progresses,  apparently 
with  degenerative  changes  in  the  muscles.  There  is,  however,  no  real 
nerve  paralysis,  but  rather  a  muscular  inefficiency  due  to  the  rigidity 
and  not  accompanied  with  degenerative  electrical  reactions.  Tlie 
innervation  of  the  facial  muscles  is  weakened  and  the  movements  slow 
so  that  the  face  becomes  smooth  and  expressionless  and  mask-like. 
The  muscles  are  overirritable  to  mechanical  irritation  and  the  facial 
responses  to  blows  are  exaggerated.  The  voice  in  paralysis  agitans  al- 
ways becomes  affected.  It  grows  weaker,  the  singing  power  is  lost,  then 
capacity  to  talk  long  or  loud.  The  lawyer  has  to  give  up  trying  cases. 
Speech  is  slow,  difficult  and  the  voice  high-pitched,  feeble  and  piping. 
Examination  shows  sometimes  tremulous  movement  of  the  cords,  but 
more  characteristic  is  the  slow,  weak  movement  of  the  cords.  In  other 
words,  the  intrinsic  muscles  become  weak  and  stiff  and  a  little  tremulous 
like  the  other  muscles  of  the  body. 

The  handwriting  in  paralysis  agitans  soon  shows  characteristic 
features.  The  act  of  writing  becomes  difficult;  the  letters  are  formed 
slowly  and  painfully;  they  are  drawn  rather  than  written.  The  letters 
get  smaller  and  more  imperfect.  Sometimes  the  writing  is  distinctly 
tremulous;  more  often  the  characteristic  is  smallness  and  lack  of  finish 
of  the  lines,  the  letters  finally  becoming  obscured.  From  year  to  year 
the  words  are  written  more  imperfectly  and  in  smaller  letters.  Tremu- 
lousness,  slowness,  lack  of  finish  of  letters  and  progressive  micrographia 
are  the  characteristic  traits. 

The  eye  movements  share  the  general  tendency  to  functional  arrest. 
The  patient  stares  steadily  ahead.     Lateral  movements  both  of  the  eyes 


572  DISEASES    OF    THE    NERVOUS    SYSTEM 

and  of  head  are  difficult.  But  the  vision  remains  good,  and  with  glasses 
the  patient  continues  to  read  though  convergence  is  tiring.  The  sensory- 
nerves  do  not  become  involved  except  that  pains  of  a  neuritic  or  aching 
and  rheumatic  character  occur.  An  initial  attack  of  sciatica  or  brachial- 
gia  is  not  uncommon.  The  muscular  sensibility  is  exaggerated.  This 
cause  a  feeling  of  restlessness  that  is  very  annoying.  The  vasomotor 
system  is  lacking  in  tone  and  stability.  A  characteristic  flush  early  shows 
on  the  cheeks  of  the  patient.  The  skin  is  ruddy,  there  is  a  tendency  to 
sweats,  and  sensations  of  heat  are  often  noted.  The  patient  likes  a 
cool  room.  The  spinal  centres  are  gradually  weakened.  Constipation 
is  the  rule;  sexual  power  is  gradually  lost;  the  bladder  after  some  years 
becomes  irritable  and  there  is  a  sense  of  frequent  desire  to  micturate. 
This,  of  course,  occurs  often  in  the  older  cases,  but  it  is  a  vesical  not  a 


^yfC^^,^^  .-^-^^C^^-^ 


Fig.  243. — Showing  progressive  micrography.     Above,  handwriting  in  1900;   below 
handwriting  seven  years  later. 

Fig.  244. — Showing  tremor  in  paralysis  agitans. 

prostatic  trouble.  Examination  shows  a  congested  condition  about  the 
neck  of  the  bladder. 

The  patient  is  often  emotional,  but  the  mind  is  not  seriously  affected. 
The  urine  is  usually  about  normal,  but  contains  an  excess  of  phosphates. 
There  may  be  polyuria  and  less  often  glycosuria. 

Forms. — A  not  very  uncommon  type  is  one  with  a  great  deal  of 
tremor  and  hardly  any  rigidity,  at  least  not  until  very  late  in  the  disease. 
About  equally  common  is  the  type  ''without  tremor"  and  with  rigidity, 
limitation  of  movements  and  deforming  attitude  alone.  Almost  always 
even  in  these  cases  a  little  tremor  is  sometimes  seen.  Unusual  types  of 
paralysis  agitans  are  the  hemiplegic  or  the  monoplegic,  and  the  retrocollic 
type. 

Course  and  Duration. — The  disease  slowly  but  steadily  progresses 
until  a  full  development  of  symptoms  occurs,  when  it  may  remain  sta- 


PAEALYSIS    AGITANS  573 

tionary.  It  takes  about  two  years  for  the  whole  body  to  be  affected, 
though  this  varies  much.  It  lasts  from  three  to  twelve  years  or  even 
more.  In  three  cases  of  mine,  death  occurred  in  three,  six,  and  eleven 
years.  Death  is  due  to  exhaustion  and  may  be  preceded  by  what 
seems  like  a  toxic  delirium  with  perhaps  some  fever. 

The  diagnosis  must  be  made  from  senile  tremor,  multiple  sclerosis, 
post-hemiplegic  tremor,  writers'  cramp  and  wry-neck  affecting  the  ex- 


-v\\^ 


:Ss$^' 


^<"r^y**  - 


Fig.  245. — Muscular  changes  in  late  paralysis  agitans. 

tensors  bilaterally  (retrocollic  spasm).  Senile  tremor  occurs  in  the 
old.  It  affects  the  head  and  there  is  no  rigidity.  In  multiple  sclerosis 
the  tremor  is  more  jerky  and  is  a  tremor  of  intention;  there  are 
nystagmus,  syllabic  speech,  and  often  apoplectiform  attacks,  eye  trouble, 
and  paralyses. 

Post-hemiplegic  tremor  is  accompanied  by  a  history  of  hemiplegia; 
there  are  paralysis  and  exaggerated  reflexes  and  the  disease  is  unilateral. 
The  absence  of  exaggerated    reflexes,  the  peculiar  voice,  gait  and  at- 


574  DISEASES    OF    THE    NEEVOUS    SYSTEM 

titude,  and  the  sensations  of  heat  and  nervousness  often  help  greatly 
in  the  diagnosis. 

The  prognosis  is  favorable  as  regards  life ;  unfavorable  as  regards 


4 

\ 

''-"■«>  ""f- 

'"^w^ 

1  V* 

lii    : 

4    - 

', 

1^ 

,-// 

"'• 

"-'  J 

<:zM^^^' 

/ 

/ 

i, 

i 

Fig.  246. — Cells  of  the  anterior  horn  of  the  spinal  cord.  The  right  row  from  a 
case  of  paralysis  agitans,  showing  atrophy  and  pigmentation,  the  left  row  from  a 
normal  case. 

cure,  and  not  very  good  as  to  bringing  about  a  cessation  of  progress  in 

the  symptoms.     The   progress  of  the   malady,  however,  can  be  delayed. 

Pathological   Anatomy    and    Pathology. — The    post-mortem  changes 

are  not  very  marked,  and  are  seen  mostly  in  the  spinal  cord  and  brain- 


PARALYSIS    AGITANS  575 

stem.  There  are  congestion  and  dilatation  of  vessels  in  the  gray  matter, 
a  diffuse  increase  of  interstitial  tissue,  atrophy  and  pigmentation  of 
cells.  The  disease  has  yet  no  established  pathological  anatomy.  De- 
generative lesions  have  been  found  in  the  anterior  cornual  cells  of  the 
spinal  cord,  and  these  resemble  somewhat  those  of  senility,  but  the  trouble 
cannot  be  explained  as  just  a  premature  senility  of  the  peripheral  neurons, 
for  extreme  old  age  does  not  present  the  picture  of  paralysis  agitans. 
Degenerative  changes  have  been  found  in  the  muscles,  but  these  are 
probably  secondary  and  it  is  not  possible  to  explain  the  vasomotor 
disturbance,  the  mental  disturbances  or  even  the  tremor  by  a  muscular 
lesion  alone.  The  disease  seems  to  impair  first  the  automatically 
acquired  activities,  so  that  to  do  an  accustomed  act  like  writing  requires 
a  distinct  and  persistent  voluntary  effort.  This  would  lead  one  to  think 
that  the  trouble  was  at  the  point  of  co-operation  between  the  voluntary 
and  the  automatic  mechanism.  The  tremor  and  rigidity,  without 
evidence  of  pyramidal  disease,  point  also  to  this  region  and  the  extra- 
pyramidal tracts.  And  in  old  cases  at  least  definite  degenerations  are 
found  in  these  tracts. 

It  is  still  unknown  whether  the  exciting  cause  of  the  functional 
degeneration  is  a  glandular  defect,  an  infection,  or  a  toxin. 

Dr.  Thos.  W.  Hastings  has  made  careful  studies  of  the  blood  in 
seven  personal  cases  of  mine.  In  four  of  them  evidences  of  infection  by 
gonococcus  or  a  micrococcus  or  both  were  found. 

Treatment. — -The  most  important  measure  is  rest,  mental  and  phys- 
ical, with  plenty  of  fresh  air.  No  special  diet  is  indicated.  Hot  baths 
and  mild  massage  are  agreeable  and  helpful.  I  know  of  no  climatic 
cure.  The  galvanic  current  produces  temporary  relief;  it  should  be 
given  daily.  Hyoscine  hyclrobromate,  first  used  by  Charcot  and  in- 
troduced into  this  country  by  Seguin,  is  of  much  value  in  relieving  the 
tremor  (gr.  3^1^0  0  increased).  Codeine  and  morphine  are  of  help  if  used 
carefully.  A  fairly  good  dose  given  once  in  the  morning  may  be  tried. 
Quinine  and  mineral  acids  are  of  much  service  in  relieving  the  vasomotor 
and  sensory  symptoms.  Bromide  often  helps  the  insomnia  and  restless- 
ness. Polyvalent  vaccines  and  injections  of  neo-salvarsan  are  being 
tried.  Full  doses  of  asafoetida  sometimes  help.  The  mind  in  paralysis 
agitans  is  sometimes  in  an  emotional,  almost  hysterical  condition,  and 
patients  are  easily  made  better  for  a  time  by  some  psychical  influence. 
Violent  exercise  does  harm.  Regular  systematic  training  exercises  do 
some  good,  vibration  is  useless  and  so  are  hypnotism  and  osteopathy. 


CHAPTER  XXVIII 
TROPHIC   AND    VASOMOTOR   DISORDERS 

Progressive  facial  hemiatrophy  is  a  disease  characterized  by  a  pro- 
gressive wasting  of  one  side  of  the  face. 

Etiology. — It  begins  oftenest  in  the  young  between  the  ages  of  ten 
and  twenty.  Females  are  more  affected.^  There  is  in  rare  cases  a 
hereditary  history.  Injury  and  infectious  fevers  sometimes  start  up 
the  trouble.     The  left  side  is  oftener  attacked. 

Symptoms. — The  disease  begins  very  gradually  and  shows  itself 
first  in  patches.     The  skin  gets  thinner,  there  is  loss  of  pigment,  hairs 


Fig.  247. — Facial  hemiatrophy,  early  stage,  showing  alopecia  and  osseous  depressions. 

fall  out,  including  those  of  the  lids  and  the  areas  may  have  a  yellowish 
appearance.  Sometimes  the  periosteum  and  bone  are  affected,  and 
shallow  depressions  are  formed  which  may  be  anaesthetic  (Fig.  248). 
The  subcutaneous  tissue  is  most  involved,  the  muscles  suffer  least,  and 
there  are  no  changes  in  electrical  reaction.  The  muscles  of  mastication 
are  usually  spared.  The  bone  undergoes  general  atrophy  and  the  lower 
jaw  may  be  reduced  to  two-thirds  the  normal  size.  The  secretion  of 
sebum  ceases,  but  that  of  sweat  may  be  increased.  The  temperature 
falls.     There  are  a  sinking  in  of  the  eye,  narrowing  of  the  lid,  and  dilata- 

1  About  one  hundred  cases  have  been  reported.  Among  five,  seen  by  myself, 
three  were  in  females,  two  in  males.  The  disease  in  all  cases,  so  far  as  could  be  found, 
began  between  the  tenth  and  twentieth  years. 

576 


PARALYSIS    AGITANS 


577 


tion  of  the  pupil.  There  is  sometimes  pain  and  rarely  anaesthesia.  The 
tongue  and  very  rarely  the  shoulder-girdle  or  the  other  side  of  the  face 
may  be  involved. 

Spasmodic  movements  of  the  muscles  of  mastication  have  been 
noted  (B.  Sachs).  Scleroderma 
sometimes,  appears  on  the  face  or 
hands.  The  trouble  may  be  com- 
plicated with  other  diseases  of  the 
nervous  system,  such  as  epilepsy, 
myoclonia  and  psychoses. 

The  disease  progresses  rather 
rapidly  at  first,  but  finally  comes 
to  a  standstill.  It  does  not  shorten 
life. 

Pathology. — There  has  been 
found  a  degenerative  neuritis  in- 
volving the  fibres  of  the  trigeminus 
and  its  descending  root.  The  weight 
of  evidence  is  in  favor  of  the  trouble 
being  due  to  disease  of  the  upper 
cervical  sympathetic. 

The  diagnosis  is  easy.  Hemi- 
plegia  with    atrophy  in   children, 

congenital  asymmetry,  and  atrophy  from  gross  lesions  of  the  nerve  are 
distinguished  by  their  stationary  character  or  the  presence  of  severe  pain. 
Treatment. — There  is  no  treatment  known  to  be  of  service.  Tonics, 
iodides,  and  electricity  may  be  tried.  Dercum 
has  suggested  resecting  the  trigeminal  nerve.  It 
would  be  worth  while  investigating  surgically  the 
superior  cervical  ganglion. 

Progressive  facial  hemihypertrophy  is  an  ex- 
tremely rare  condition  only  eleven  cases  having 
been  reported.  It  is  usually  congenital  in  origin, 
but  may  develop  in  connection  with  giantism,  as 
in  a  case  of  my  own  (Fig.  249). 


Fig.  248. — Facial  hemiatrophj^ 
born  and  Krieger.) 


(Schoen- 


FiG.  249.  — Facial 
hemihypertrophy  oc- 
curring in  a  giant. 


DISEASES  OF  THE  PITUITARY  GLAND 


The  pituitary  gland  is  composed  of  an  anterior 
part  derived  from  the  buccal  ectoderm  which  has 
to  do  with  nutritive  changes  and  the  development  when  diseased  of 
acromegaly  and  giantism;  a  pars  intermedia  which  produces  a  substance 
that  stimulates  unstriped  muscle,  produces  diuresis  and  secretes  a  prod- 
uct which  passes  into  the  cerebral  ventricles  and  has  some  influence  on 


578 


DISEASES    OF    THE    NERVOUS    SYSTEM 


the  growth  and  functions  of  the  nervous  system;  a  posterior  part 
which  consists  mainly  of  neurogha.  Feeding  the  anterior  part  to  young 
animals  seems  to  stimulate  growth.  The  posterior  lobe  extract  has  no 
physiological  effect.  The  pineal  gland  seems  to  have  somewhat  anal- 
ogous functions. 

Pathological  and  Physiological  Effects  Attributed  to  the  Activities  or 

Disorders  of  the 


Pituitary  body 


Pineal  body 


Adiposity. 

Sexual  changes. 

Genital  atrophy  and  infantilism. 

Acromegaly  and  gigantism. 

Polyuria. 

Control  of  carbohydrate  metabolism. 

Lowered  temperature. 

Co-ordinate  action  with  other  glands. 

Physiological  action  of  extract  of  the 
gland. 

Pressor  and  depressor  effect  on  blood- 
vessels. 

Galactagogic  effect. 

Stimulation  of  muscles  of  pupil,  uterus 
and  intestines. 

Modifications  of  metabolism  and  bodily 
growth. 

Modification  of  carbohydrate  metabolism. 


Adiposity  (later  sometimes  a  marked 
atrophy  of  fatty  tissues). 

Early  development  of  sexual  organs  and 
functions. 

Early  bodily  and  mental  maturity  (Macro- 
genitosomia of  Pellizi). 

Physiological  action  of  extracts  of  the  gland. 

Contradictory  reports  as  to  pressor  and 
depressor  effect  on  blood-vessels. 

Stimulation  of  unstriped  muscular  tissue 

of  intestines,  uterus,  pupil. 
Vasodilatation  of  genitalia  and  kidney. 
Transitory  diuresis. 

Glycosuria. 

Stimulation  of  metabolism  (Berkeley). 


Three  disorders  are  recognized  clinically  as  due  to  disease  of  the  pitui- 
tary gland;  giantism,  acromegaly,  and  the  Frohlich  syndrome,  a  condition 
characterized  by  stunting  of  growth,  adiposity,  and  hypoplasia  of  the 
genitals  (Fig.  250). 

Acromegaly  is  a  chronic  dystrophy  characterized  by  gradual  enlargement  of  the 
hands,  feet,  head,  and  thorax,  and  by  a  dorso-cervical  kyphosis. 

Etiology. — It  affects  the  two  sexes  nearly  alike.  It  begins  between  the  ages  of 
eighteen  and  twenty-six,  although  a  congenital  case  has  been  reported.  No  hereditary 
influence  or  definite  exciting  cause  is  known.  The  patients  are  sometimes  naturally 
endowed  with  large  extremities. 

Symptoms. — The  disease  begins  with  a  gradual  enlargement  of  the  bones  and 
soft  parts  of  the  hands,  feet  and  head,  including  the  nose,  lips  and  jaws.  In  women 
there  is  amenorrhoea,  in  men,  sexual  weakness;  slight  rheumatic  pains,  headaches, 
malaise,  mental  hebetude,  anaemia,  and  general  weakness  are  present.  The  patient 
shows  striking  contrast  between  his  bulk  and  his  general  strength.  The  skin  is 
dry  and  there  is  polyuria. 

The  hypertrophy  affects  the  soft  parts  as  well  as  bones.  In  these  latter  there  are 
periosteal  thickening  and  hyperplasia,  with  the  result  of  producing  increase  in  width 
more  than  length.     The  arms  are  not  much  involved,  nor  is  the  shoulder-girdle,  except 


TROPHIC    AND   VASOMOTOR    DISORDERS 


579 


the  clavicle.  The  lower  jaw  is  much  more  involved  than  the  cranium.  The  tongue, 
lips  and  nose  are  enormously  hypertrophied  (Fig.  251) .  The  thorax  is  enlarged  antero- 
posteriorly  and  flattened.  There  is  characteristic  cervico-dorsal  kyphosis.  There  is 
sometimes  dullness  over  the  sternum  due  to  persistence  of  the  thymus.  The  pelvis 
may  be  enlarged,  but  the  hip  and  leg  bones  are  generally  spared.  The  hands  and  feet 
undergo  enormous  hypertrophy  (Fig.  252).  The  following  are  some  of  the  measure- 
ments in  the  case  that  has  come  under  my  observation,  reported  by  Adler,  and  in 
cases  reported  by  Osborne  and  Packard: 


Fig. 


250. — Frohhch  syndrome.     Tumor  of  hypophysis  in  boy  of  twelve.     Adiposity, 
[defective  development  of  genitals;  choked  discs,  headache,  nystagmus. 


Length  of  hand 7 . 6  to    8^  inches. 

Length  of  foot 11.7  to  123^^  inches. 

Cranial  circumference 24      to  263''7  inches. 

Circumference  of  thorax 44  inches. 


The  whole  body  may  take  part  in  the  growth  and  some  giants  have  acromegaly, 
if  the  disease  begins  quite  early  in  life. 

There  may  be  vasomotor  and  cardiac  disturbances. 

Headache,  and  symptoms  of  brain  tumor  may  develop  owing  to  the  enlarging 
pituitary  body.  The  patient's  mind  usually  becomes  dull  and  apathetic.  Disorders 
of  metabolism  occur  with  bulimia,  and  glycosuria.  The  vision  is  sometimes  impaired 
and  there  may  be  temporal  hemianopsia  due  to  the  pressure  of  the  enlarged  pituitary 


580  DISEASES    OF    THE    NERVOUS    SYSTEM 

bodj^  on  the  optic  chiasm.  Ocular  palsies  may  occur.  The  muscles  may  be  at  first 
hypertrophied.  later  atrophied.     There  are  no  paralyses  and  rarely  any  anaesthesise. 

The  disease  runs  a  very  chronic  course,  lasting  ten  or  twenty  years. 

Pathology. — There  has  been  found  an  enlargement  of  the  pituitary  body  in  nearly 
all  cases,  and  it  is  probable  that  the  disease  is  to  be  regarded  as  a  perversion  of 
nutrition  accompanied  by  hypertrophy  and  defective  function  of  the  pituitary 
gland. 


Fig.  251. — Acromegaly. 

If  pituitary  disease  begins  before  the  epiphyses  of  the  long  bones  are  united 
there  may  be  giantism;  if  it  begins  later,  acromegaly. 

The  diagnosis  must  be  made  from  congenital  enlargements,  from  so-called  giant 
growth  which  affects  single  members,  and  from  osteitis  deformans.  In  the  latter 
disease  it  is  the  shafts  of  the  long  bones  and  the  cranium,  not  the  face,  which  are 
involved. 

Prognosis. — Acromegaly  is  incurable,  but  it  has  been  arrested,  or  at  least  has 
ceased  to  progress,  and  it  may  not  greatly  shorten  life. 

Treatment. — Cases  have  been  reported  in  which  iodide  of  potassium  and  arsenic 


TKOPHIC    AND   VASOMOTOR    DISORDERS  581 

have  arrested  the  disease.  In  general,  the  treatment  is  only  symptomatic,  but  feeding 
with  pituitary  gland  has  been  tried,  and  it  sometimes  does  good.  Removal  of  a  portion 
of  the  gland  by  the  surgeon  may  be  required  on  account  of  the  development  of  neigh- 
borhood symptoms.     The  use  of  X-ray  and  of  radium  is  now  being  tested. 

MYXCEDEMA 

Myxoedema  is  a  disease  of  the  thyroid  gland,  but  its  sjaiiptoms 
are  so  largely  nervous  and  mental  that  a  brief  description  of  it  is  justified 
here.  It  is  a  chronic  disorder,  due,  as  a  rule,  to  an  interstitial  thyroiditis, 
and  characterized  by  a  solid  oedema  of  the  subcutaneous  tissue,  dry 
skin,  loss  of  hair,  subnormal  temperature,  mental   dullness,  and  even 


Fig.  252. — Hand  in  acromegaly. 

insanity  and  idiocy.  It  has  two  forms — the  congenital  and  infantile 
— causing  a  condition  known  as  cretinism ;  and  an  adult  form  constituting 
myxoedema  proper. 

It  occurs  most  often  between  the  ages  of  thirty  and  fifty,  and  oftener 
in  women  (seven  to  one).  It  is  seen  oftenest  in  temperate  climates. 
Hereditary  influence,  alcoholism,  and  syphilis  are  not  predisposing 
factors;  lead  poisoning  may  be  a  cause. 

It  begins  slowly.  The  patient  is  languid  and  dull,  and  is  unusually 
sensitive  to  cold.  Voluntary  movements  are  slow;  the  weight  increases 
and  a  solid  oedema  which  does  not  dent  on  pressure  develops  in  the 


582 


DISEASES    OF    THE    NEEVOUS    SYSTEM 


face  and  extremities.  The  skin  gets  dry  and  rough,  the  hair  begins 
to  fall,  the  temperature  is  subnormal,  1°  to  2°F.  Mentally  the  patient 
is  dull,  depressed,  and  in  one-fifth  of  the  cases  melancholia,  mania,  or 
dementia  develop.  The  muscles  are  weak,  the  gait  is  slow,  the  voice 
hoarse  and  monotonous.  There  is  considerable  anaemia  and  the  heart 
is  weak.  The  pulse  is  slow  and  the  arterial  tension  low.  Albuminuria 
is  present  in  20  per  cent,  of  cases,  and  hemorrhages  may  occur. 

The  pallor,  oedema,  loss  of  hair,  and  mental  hebetude  give  to  the 
face  a  characteristic  expression  (Fig.  253).  The  disease  may  run  a 
course  of  six  or  seven  years,  the  patient  dying  of  cardiac  weakness  or 
some  intercurrent  malady. 


riG.'^253. — A  case  of  myxoedema  in  a  man  aged  forty-four  years.     {Murray.) 


The  disorder  is  due  in  most  cases  to  a  chronic  interstitial  thyroiditis 
which  ^usually  causes  atrophy  of  the  gland.  It  may  be  produced  by 
artificial  removal  of  the  thyroid.  The  result  of  this  is  a  defective  action 
of  the  thyroid,  and  a  consequent  poisoning  of  the  system  and  deposit 
of  mucin  in  the  subcutaneous  tissue  especially. 

The  diagnosis  is  based  upon  the  peculiar  physiognomy  due  to  the 
oedema,  the  loss  of  hair,  subnormal  temperature,  mental  hebetude,  and 
atrophied  thyroid. 

The  prognosis  is  good  if  treatment  is  instituted  early. 


TROPHIC    AND   VASOMOTOR    DISORDERS 


583 


The  treatment  consists  in  the  administration  of  the  thyroid  ex- 
tract in  daily  doses  ranging  from  five  to  forty  grains  or  even  more. 
The  results  are  most  brihiant,  and  humanity  owes  much  to  Dr.  George 
R.  Murray,  who  first  instituted  it. 

CRETINISM 

Cretinism  is  a  form  of  myxoedema  due  to  atrophy,  or  defective 
functioning  of  the  thyroid  gland,  occurring  congenitally  or  during 
infantile  life.  The  disease  occurs  endemically  in  parts  of  Europe,  but 
only  sporadically  and  with  great  rarity  in  America.  Hereditary  and 
family  influences  are  at  work  in  endemic  but  not  in  sporadic  cretin- 
ism. It  develops  either  directly  after  or  in  the  first  three  years 
of  life,  and  shows  itself  in  a  stunted  growth  both  of  brain  and  body, 
most  cretins  being  idiotic  dwarfs.     The  general  symptoms  are  much 


Fig.  254. — A  cretin  dwarf,  aged  twenty.     (Leszynsky.) 

like  those  of  myxoedema  in  adults  plus  the  retarded  growth  of  mind  and 
body.  The  deposits  of  solid  oedema  cause  peculiar  deformities  and  lead 
to  a  characteristic  physiognomy.  The  mind  is  dull  and  placid,  the 
muscles  are  weak,  the  abdomen  is  protuberant,  the  hands  and  feet  are 
broad  and  thick;  the  patients  are  anaemic,  the  temperature  is  subnormal. 
The  arrested  bodily  growth  is  such  that  on  reaching  adult  age  the  stature 
may  be  only  twenty-eight  to  thirty-three  inches. 

Cretins  usually  die  young,  but  some  survive  to  the  age  of  thirty  and 
forty. 

The  treatment  is  the  same  as  that  of  myxoedema.  Here,  too,  if 
the  case  is  seen  before  adolescence,  brilliant  results  can  be  obtained. 

ANGIO-NEUROTIC  (EDEMA 

(Circumscribed  (Edema;  Quincke's  Disease,  (Edema  Fugax) 

Angio-neurotic  oedema  is  a  disorder  characterized  by  the  rather  rapid 
appearance  of  circumscribed  and  temporary  swellings  of  the  skin  and 


584  DISEASES    OF    THE    NERVOUS    SYSTEM 

subcutaneous  tissue,  and  of  the  mucous  membrane.  The  swellmgs 
appear  upon  different,  generally  exposed  parts  of  the  body.  The  mucous 
membranes,  especially  those  of  the  respiratory  and  gastro-intestinal  tracts 
may  be  involved  at  the  same  time  or  independently. 

The  disease  occurs  oftenest  in  early  adult  life,  the  average  age  being 
from  twenty  to  thirty,  but  it  has  been  observed  in  young  children  and 
even  in  the  aged.  It  occurs  oftener  in  females  than  in  males.  Heredi- 
tary influence  plays  a  part  in  some  cases;  and  the  disease  sometimes 
runs  in  families.  It  occurs  in  neuropathic  individuals  and  families.  It 
is  associated  with  other  paroxysmal  neuroses  such  as  migraine,  urticaria, 
certain  forms  of  asthma,  oedematous  purpura  and  eczema.  It  occurs 
oftener  in  winter  and  oftener  in  the  early  morning  hours. 

Exhausting  occupations  predispose  to  it.  The  exciting  causes  are 
sudden  exposure  to  cold,  slight  traumatisms,  fright,  anxiety,  grief, 
and  the  ingestion  of  certain  kinds  of  food,  such  as  apples,  strawberries, 
or  fish.  A  peculiar  form  of  this  oedema  seems  to  develop  in  connection 
with  menstruation. 

Symptoms. — The  disease  appears  without  much  if  any  warning. 
In  a  few  minutes  or  hours  there  develops  a  circumscribed  swelling  upon 
the  face  or  arms  or  hands.  This  swelling  varies  in  diameter  from  one- 
half  inch  to  two  or  three  inches.  It  may  be  dark  reddish  or  rosy  or 
it  may  be  pale  and  waxy.  It  does  not  easily  pit  on  pressure.  There  is 
sometimes  a  rise,  sometimes  a  fall  in  local  temperature.  It  is  accom- 
panied by  sensations  of  tension  and  stiffness,  scalding,  burning,  and 
sometimes  itching,  but  there  is  no  actual  pain.  The  swelling  is  usually 
single,  but  it  may  be  multiple.  It  is  located  most  often  upon  the  face, 
next  upon  the  extremities,  particularly  the  hands;  next  on  the  body,  then 
in  the  larynx  and  throat,  and  then  on  the  genitals.  The  swellings 
last  from  a  few  hours  to  two  or  three  days.  Between  the  attacks  the 
patient  feels  well.  They  are  apt  to  return  at  intervals  of  three  or  four 
weeks  to  several  months.  Sometimes  they  are  brought  out  only  by  cer- 
tain peculiar  exciting  causes,  such  as  indigestion  or  mental  anxieties  or 
emotional  disturbances.  When  the  disease  attacks  the  larynx  or  throat, 
serious  symptoms  of  dyspnoea  and  suffocation  may  appear;  surgical 
interference  may  even  be  called  for,  and  death  has  been  known  to  result. 
The  oedema  may  attack  the  stomach,  producing  nausea,  vomiting,  and 
great  gastro-intestinal  distress,  or  the  intestines  causing  colic  and 
diarrhoea. 

The  pathology  of  this  neurosis  is  imperfectly  known  but  is  some- 
what as  follows: 

The  disease  is  associated  with  and  is  allied  to  a  group  of  neuroses  or 
angio-neuroses  including  migraine,  urticaria,  certain  forms  of  asthma 
and  purpura. 


TROPHIC    AND   VASOMOTOR    DISORDERS  585 

The  victim  possesses  a  constitutional  defect  which  is  sometimes 
inherited  and  transmitted.  This  defect  may  be  a  dysthyroidism,  or 
other  disorder  of  the  endocrine  cells.  It  shows  itself  in  weakness  in  the 
chemistry  and  cellular  functions  of  the  gastro-intestinal  tract,  allowing 
entrance  into  the  blood  of  heterogeneous  proteins  (anaphylaxis). 

The  incident  of  an  attack  of  oedema  (anaphylactic  shock)  is 
brought  about  by  depressing  emotions,  trauma,  shock,  exposure,  certain 
foods  ingested. 

Then  the  heterogeneous  proteid  in  the  system  attacks  the  vasomotor 
nerves  at  certain  points,  because  there  is  an  irritant  or  extra-point  of 
weakness  at  these  points.  There  follows  an  excessive  permeability  of 
the  vascular  endothelium,  and  transudate  of  serum. 

Diagnosis. — The  symptoms  of  the  typical  disease  are  so  peculiar  that 
they  are  easily  recognized.  The  spontaneous  appearance  of  the  oedema, 
its  recurrence  at  certain  intervals,  and  the  absence  of  serious  pain  and 
evidences  of  inflammation  are  sufficient  usually  to  enable  us  to  recognize 
it.  Giant  urticaria  is  a  disease  resembling  neurotic  oedema  and  prob- 
ably closely  allied  to  it.  The  blue  and  the  white  oedema  of  hysterics  only 
exists  with  other  stigmata  of  hysteria. 

The  prognosis,  so  far  as  cure  is  concerned,  is  not  very  good.  The 
attacks,  however,  can  be  ameliorated,  and  the  disease  itself  is  not  serious, 
as  regards  life  except  when  it  attacks  the  larynx.  Most  of  the  patients 
whom  I  have  seen  have  eventually  recovered. 

The  treatment  consists  in  the  adoption  of  such  measures  as  will  give 
tone  and  stability  to  the  nervous  system,  and  the  gastro-intestinal  tract. 
In  some  cases  great  attention  must  be  paid  to  diet.  Internally,  mineral 
acids  and  strychnine  may  be  of  some  value.  A  systematic  and  pro- 
longed use  of  arsenic  has  been  followed  by  cure;  urotropin  has  been 
used  with  success,  and  so  also  has  nitroglycerin,  and  horse-serum  (in  a 
case  associated  with  purpura).  The  lactate  of  calcium  5i  daily  is 
sometimes  helpful.  Gastro-intestinal  crises  may  require  morphine.  In 
laryngeal  oedema,  intubation  should  be  promptly  done.  , 


CHAPTER  XXIX 

THE  DISORDERS  OF  SLEEP 

INSOMNIA,  HYPNOTISM,  MORBID  SOMNOLENCE,  CATALEPSY,  TRANCE, 
LETHARGY,    THE    SLEEPING     SICKNESS 

The  most  conspicuous  phenomenon  of  sleep  is  the  loss  or  partial  loss 
of  consciousness.  With  this  the  regulating  mechanism  of  the  mind  is 
in  abeyance.  Mental  processes  go  on,  when  at  all,  by  free  associations 
or  in  accordance  with  the  emotional  trend  or  as  activated  by  sensory 
and  somatic  irritants. 

The  cause  of  sleep  is  not  exactly  known.  We  know  that  sleep  is  a 
normal  resting  phase  of  brain  action,  a  kind  of  cerebral  diastole.  It 
is  probable  that  the  brain  neurons  by  their  activity  throw  off  products  of 
metabolism  which  tend  to  benumb  and  inhibit  their  waking  physiological 
functioning.  It  has  been  found  that  the  brain  is  slightly  anaemic  during 
sleep,  but  this  is  part  of  the  process  not  the  cause  of  it.  Other  organs 
of  the  body  rest  somewhat  also  during  sleep,  and  especially  is  this  true  of 
the  muscular  system.  There  are  slight  changes  in  pulse,  respiration, 
blood-pressure  and  other  bodily  functions  in  sleep  but  these  are  described 
adequately  in  physiological  text-books. 

Normal  sleep  varies  much  in  accordance  with  age,  sex,  the  individual, 
and,  to  a  slight  extent,  with  occupation,  race  and  climate.  The  infant 
sleeps  at  first  nearly  all  the  time,  later  fourteen  to  sixteen  hours,  but  its 
sleep  is  light.  Young  children  sleep  ten  to  twelve  hours.  The  adult  needs 
about  eight  hours,  while  the  aged  live  healthfully  with  but  six.  Women 
need  half  an  hour  or  an  hour  more  than  men.  A  few  persons,  generally 
men,  need  nine,  ten,  or  even  twelve  hours'  sleep  daily;  others  require 
only  six.  Brain  workers,  as  a  class,  take  less  sleep  than  laborers.  Sleep 
is  sounder  and  longer  in  cold  climates  and  among  northern  races. 

The  disorders  and  perversions  of  sleep  include  insomnia,  morbid 
somnolence,  morbid  dreaming,  sleep-walking,  hypnotic  and  trance  states. 
They  are  disarrangements  of  a  normal  function,  brought  about  by  various 
causes.  Sleep  itself  may  be  the  morbid  expression  of  a  disease,  as  in 
narcolepsy,  the  sleeping  sickness  of  Africa,  and  the  somnolence  of  the 
senile  brain.  Conditions  allied  to  normal  sleep  exist  in  the  hypnotic 
and  trance  states.  Among  all  these  conditions,  practically,  insomnia 
is  the  sleep  disorder  which  most  annoys  humanity,  and  it  comes  next  to 
food  and  raiment  and  human  love  in  the  concern  of  civilized  man. 

586 


THE    DISORDERS    OF    SLEEP  587 


INSOMNIA 


Insomnia  is  a  condition  in  which  persons  suffer  from  insufficient  and 
disturbed  or  unrestful  sleep.  The  term  "insomnia"  covers  all  these 
deficiencies,  but  the  old  Roman  writers  used  the  word  exsovinia  for  a 
condition  of  excited  wakefulness,  such  as  came  with  morbid  mental 
exaltation  and  the  delirium  of  the  Bacchic  priestess. 

Insomnia  is  a  symptom  of  many  disordered  physical  and  mental  con- 
ditions, and  it  has  been  considered  elsewhere  in  connection  with  the  most 
important  of  these.  It  occurs  in  its  most  serious  and  persistent  forms  in 
painful  diseases,  in  the  psycho-neuroses,  and  in  manic  and  depressed 
states.  Here  one  sometimes  finds  cases  of  apparent  entire  absence  of 
sleep  for  prolonged  periods.  This  ahypnosis  is  not,  however,  absolute. 
Man  can  exist  without  sleep  for  about  the  same  time  that  he  can  go  with- 
out food,  viz.,  3  or  4  weeks,  but  he  cannot  live  without  it. 

Etiology. — Insomnia  of  mild  grades  occurs  often  apart  from  any 
very  serious  physical  disturbance.  It  may  be  a  hereditary  or  family 
trait  not  to  sleep  easily  or  well.  More  often  it  is  acquired  by  bad  habits 
of  life,  by  disturbing  environments,  by  anxiety  of  mind  and  by  excessive 
use  of  drugs,  tobacco,  tea  and  coffee.  It  may  be  the  result  of  endogenous 
irritants,  such  develop  in  cases  of  poor  digestion,  in  faulty  metabolism 
or  in  hyperthyroidism. 

Disease  of  the  heart  and  arteries  may  lead  to  insomnia,  and  under 
this  head  come  the  cases  which  occur  in  Bright's  disease  with  sclerotic 
arteries  and  anaemic  brains.  Disorders  of  the  stomach  lead  to  disturbed 
sleep  oftener  than  to  complete  insomnia,  and  the  liver,  when  inactive, 
causes  somnolence  rather  than  the  contrary.  Insomnia  is  a  disorder 
especially  of  the  active  periods  of  life,  though  children  suffer  from  it 
also.  In  their  case  it  is  usually  due  to  some  definite  physical  cause, 
such  as  pain,  indigestion,  emotional  excitement;  yet  one  not  infrequently 
meets  children  who  from  early  life  go  to  sleep  with  difficulty.  It  is  in 
this  period  of  life  that  the  active  and  bizarre  disorders  of  sleep  occur, 
such  as  sleep-walking,  night-mare  and  pavor  nocturnus.  The  aged  have 
insomnia  but  do  not  suffer  so  much  from  it.  Women  have  insomnia 
rather  less  than  men;  and  brain  workers  more  than  muscle  workers. 
Insomnia  is  more  common  in  cold  climates,  largely  because  there  is  more 
brain  work  done  there.  High  altitudes  tend  to  cause  insomnia,  at  least, 
till  the  system  becomes  accustomed  to  the  change. 

Anxiety  of  mind  and  brain  fatigue  lead  to  insomnia;  and  very  often 
to  the  morning  type.  The  patient  who  carries  a  worry  wakes  at  3  or 
4  A.M.  instead  of  his  usual  hour.  Insomnia  is  a  warning  symptom  of 
the  approach  of  neurasthenia  and  of  certain  mental  disorders,  especially 
melancholia  and  the  obsessive  psychoses. 


588  DISEASES    OF    THE    NERVOUS    SYSTEM 

Summary:  Insomnia  is  due  to 

1.  Hereditary  and  constitutional  conditioiis. 

2.  Habits  of  life:  of  work,  of  eating,  of  environment  and  of  too  violent 
exercise. 

3.  Irritative  conditions  such  as  pain,  pruritus,  indigestion. 

4.  Toxic  agents,  tobacco,  tea,  coffee,  cocaine,  morphine. 

5.  Endogenous  toxins,  gastro-intestinal,  glandular.' 

6.  Vascular  degenerative  disease  of  the  brain. 

7.  Psychic  causes;  fatigue,  worry,  the  onset  of  psychoses. 
Treatment. — -The  enumeration  of  the  causes  of  insomnia,  covers  a 

large  part  of  the  discussion  on  treatment.  For  treatment  involves  a 
consideration  of  the  cause,  then  the  laying  down  of  rules  of  hj^giene, 
the  arrangement  of  daily  work  and  play,  the  times  of  eating,  diet,  exercise, 
the  hours  of  retiring  and  the  amount  of  sleep  needed.  Nearly  all  these 
points  have  been  discussed  under  special  chapters.  I  shall  discuss  now 
only  certain  particular  medicines  and  measures  used  for  the  symptom 
insomnia. 

The  older  physicians  in  treating  sleeplessness,  used  to  depend  largely 
on  hyoscyamus,  camphor,  opium,  and  the  fetid  drugs,  such  as  asafcetida, 
musk,  and  valerian.  Hyoscyamus  is  still  used.  The  hydrobromate  of 
hyoscine,  in  doses  of  gr.  3^foo  to  gr.  i^^q  or  more,  is  the  best  form. 
Hyoscine  is  indicated  in  the  insomnia  of  delirium  and  mania  which  is 
accompanied  by  motor  activity.  Chloral  hydrate  still  holds  its  own  as 
one  of  the  surest  of  hypnotics.  The  dangers  involved  in  its  use  have  been 
somewhat  exaggerated,  though  thej^  are  sufficiently  real.  Doses  of  gr. 
X.  and  gr.  xv.  are  often  quite  large  enough,  but  in  alcoholic  insomnia 
it  may  be  given  in  twice  the  above  amounts,  guarded  with  ammonia  and 
digitalis. 

Bromide  is  one  of  the  best  hypnotics  but  it  has  to  be  skilfully  used. 
The  immediate  effect  is  simply  sedative,  and  sleep  is  not  produced  unless 
large  doses  are  given.  Some  persons  are  even  kept  awake  by  average 
doses  (gr.  xv.  to  xx.).  In  insomnia,  therefore,  bromides  are  best  pre- 
scribed in  doses  of  gr.  xxx.  twice  in  the  evening  for  not  over  four  days. 
By  the  third  evening  sleep  is  generally  secured.  A  bromide  habit  is  rarely 
formed,  and  is  in  itself  not  seriously  injurious.  The  bromides  alone  are 
hardly  strong  enough  hypnotics  for  the  insomnia  of  delirium  and  mania 
and  they  are  not  so  efficient  in  the  weak  and  aged.  Paraldehyde  ranks 
close  to  chloral  in  its  value  as  a  hypnotic.  In  some  persons  it  disturbs 
the  stomach,  but  not  in  all,  and  it  may  be  used  as  a  hypnotic  for  months 
without  its  power  being  impaired.  It  is  a  disagreeable  drug,  and  there  is 
nothing  so  far  as  I  know,  that  palliates  its  offensiveness.  I  prefer, 
however,  to  prescribe  it  in  5i-  doses  poured  upon  a  teaspoonful  of  pow- 


THE    DISORDERS    OF    SLEEP  589 

dered  sugar.  The  paralydehyde  habit  may  be  formed  and  it  is  bad  Hke 
all  drug  habits,  but  less  serious  than  chloral  or  opium  addiction. 

Amylene  hydrate  is  a  hypnotic  of  properties  similar  to  those  of 
paraldehyde,  but  less  disagreeable.  It  is  given  in  doses  of  about  one 
drachm.  Lupulin  in  large  doses,  gr.  x.  to  gr.  xx.  is  a  fairly  good  hyp- 
notic. Chloralamide  is  more  agreeable  than  chloral,  though  it  acts 
practically  in  the  same  way.  Sulphonal,  trional,  veronal,  medinal  and 
adalin,  all  act  in  much  the  same  way;  but  vary  in  strength  and  quickness 
of  absorption  and  elimination. 

Among  the  antispasmodics  are  several  drugs  which  occasionally 
answer  well  in  the  insomnia  due  to  nervous  irritability.  For  example, 
tincture  of  valerian  and  spirits  of  lavender  are  sometimes  adequate  as 
sleep  inducers.  Ten  grains  of  aspirin  act  sometimes  as  a  harmless 
hypnotic.  A  bottle  of  beer,  or  a  drink  of  whiskey  are  hypnotics  but 
are  dangerous  medicines,  for  their  effects  wear  off  and  larger  doses  are  soon 
demanded.  Safer  measures  are  the  taking  of  digestive  food  just  before 
retiring  or  on  too  early  waking.  A  glass  of  hot  milk  or  hot  malted  milk 
often  works  successfully. 

Besides  drugs,  there  are  many  hygienic  or  mechanical  measures 
to  which  the  physician  may  successfully  resort — -listening  to  monoto- 
nous noises,  reading  dull  or  heavy  books,  counting,  or  keeping  before 
the  fancy  some  blank  or  wearying  picture — ■ 

"A  flock  of  sheep  that  leisurely  pass  by 
One  after  one;  the  sound  of  rain  and  bees 
Murmuring;  the  fall  of  rivers,  winds  and  seas, 
Smooth  fields,  white  sheets  of  water,  and  pure  skies." 

In  cases  of  purely  bad  habit  insomnia,  psycho-therapeutics  even 
to  the  point  of  actual  hypnosis  may  be  tried. 

Mechanical  remedies  have  nearly  all  for  their  purpose  the  with- 
drawal of  the  blood  from  the  brain  to  the  skin  and  abdominal  viscera. 
Hot  footbaths  or  warm  general  baths,  cold  douches  down  the  spine, 
abdominal  compresses,  beating  the  limbs  with  rubber  hammers,  massage, 
all  are  at  times  efficient  hypnotics.  Persons  who  suffer  from  insomnia 
should  sleep  in  cold  rooms,  the  head  should  not  be  too  high  or  very  low, 
and  in  most  cases  they  are  better  without  late  suppers,  even  though  these 
be  light.  Mental  work  should  be  laid  aside  several  hours  before  retiring 
and  the  evening  devoted  to  quiet  conversation  and  reading  or  amusements 
that  do  not  actively  excite  the  nerves.  Many  persons  live  in  good  health 
though  they  sleep  in  the  day  and  stay  awake  at  night.  Despite  this,  it 
is  true  that  the  best  time  for  sleep  is  at  night,  and  that  the  old  maxim, 
"Early  to  bed,"  is  a  sound  one.  Yet  it  is  not  the  early  bird  that  gets 
the  Avorm  so  much  as  the  bird  that  has  slept  enough.     The  human  system 


590  DISEASES    OF    THE    NERVOUS    SYSTEM 

requires  a  certain  amount  of  sleep  and  should  have  it.  The  industrious 
and  ambitious  often  try  to  train  themselves  to  shorter  hours,  but  though 
they  may  succeed  for  a  time,  nature  will  not  be  cheated  out  of  her  due  and 
health  suffers  in  the  end.  It  is  a  widespread  custom  in  some  countries  to 
take  a  short  nap  in  the  daytime,  and  the  custom  is  a  good  one,  for  the 
weak  and  aged  and  over-worked. 

In  early  life,  at  least,  a  habit  of  going  to  sleep  when  desired  can  be 
formed  by  careful  attention  and  exercise  of  the  will.  It  is  a  most  useful 
asset  throughout  life. 

PERVERSIONS  AND  DISTURBANCES  OF  SLEEP 

Sleep  is  said  to  reach  its  deepest  stage  in  from  one  to  two  hours  after 
it  begins.  There  is  then  after  this  a  gradual  lessening  of  the  depth  of 
sleep.  Probably  there  are  great  variations  in  this  rule,  for  many  persons 
seem  in  soundest  slumber  several  hours  after  falling  asleep.  But,  at  any 
rate,  there  are  lighter  stages  of  sleep  at  its  inception  and  toward  its  end. 
These  are  the  favorite  times  for  dreams,  and  at  this  period  also  there 
develop  the  peculiar  phenomena  of  sleep-drunkenness. 

Dreams. — When  sleep  is  perfect  and  profound,  dreams  afterward  re- 
membered do  not  occur.  Dreaming  is,  therefore,  a  morbid  symptom, 
although  often  of  trivial  significance,  especially  if  it  occurs  at  about 
the  time  of  natural  waking,  when  slumber  is,  in  its  physiological  course, 
passing  into  the  lighter  stages.  In  sleep,  no  matter  how  light,  the 
action  of  the  regulating  centre,  which  directs  thought,  controls  einotion, 
and  exhibits  itself  in  volition,  is  suspended;  the  physical  mechanism, 
if  excited  to  action  at  all,  works  without  purpose,  like  a  rudderless  ship 
at  sea.  Ideas  and  emotions  succeed  each  other  by  the  laws  of  associa- 
tion, but  are  not  properly  correlated,  and  judgment  and  logical  reasoning 
are  gone.  As  a  rule,  dreams  are  made  up  of  somewhat  ordinary  ideas 
and  fancies  incoherently  associated,  and  shifting  too  rapidly  to  call  up 
much  feeling.  AVhen  from  some  point  in  the  body  painful  sensory  ex- 
citations do  produce  disagreeable  images,  emotions  of  a  most  violent 
kind  may  be  felt. 

The  Freudian  interpretation  of  the  dream  as  expressing  symbolically 
or  otherwise  a  wish  is  one  that  does  not  concern  the  clinician  unless 
he  believes  in  the  value  of  psycho-analysis. 

Nightmare  is  a  disorder  nearly  always  symptomatic  of  an  irritation 
in  some  part  of  the  body.  The  usual  causes  of  it  are  some  digestive 
disturbance  (repletion)  and  cardiac  disease.  Persons  of  a  nervous  tem- 
perament are  more  subject  to  it;  and  there  are  individuals  who  suffer 
from  it  all  their  lives.  The  popular  belief  that  sleeping  on  the  back  favors 
it  is,  in  general,  a  correct  one.     When  nightmare  occurs  in  cardiac  disease 


THE    DISORDEKS    OF    SLEEP  591 

a  certain  position,  semirecumbent  or  on  the  right  side,  must  be  main- 
tained, or  the  painful  fancies  will  awaken  the  patient.  Healthy  people 
can  get  sound  sleep  whether  lying  upon  the  back,  the  side,  or  the  stomach ; 
but  light  sleepers,  and  those  with  sensitive  abdominal  viscera,  generally 
find  that  the  position  on  the  right  side  is  the  most  comfortable  and  less 
provocative  of  unpleasant  dreams.  Prolonged  mental  or  physical  strain, 
excitement,  and  worry,  predispose  to  nightmare.  A  high  proteid  diet, 
excess  of  sweets  in  diet,  excessive  use  of  strong  liquors,  coffee  and  tobacco, 
have  a  similar  tendency. 

Pavor  nocturnus,  or  night-terrors,  is  a  sleep  disorder  peculiar  to 
children.  It  is  allied  to  nightmare  on  the  one  hand  and  sleep-drunken- 
ness on  the  other.  It  differs  from  the  former  condition  in  that  the 
child  continues  to  suffer  from  the  distressing  fancies  for  some  time 
after  he  is  awake.  Night-terrors  occur  usually  one  or  two  hours  after 
sleep  has  begun.  The  child  wakes  up  screaming  with  fright,  and  per- 
haps runs  about  the  room  or  seeks  its  parents  for  protection  against 
some  imagined  harm.  The  disorder  occurs  in  weakly,  anaemic,  nervous, 
or  rheumatic  children.  It  is  due  sometimes  to  what  has  been  termed 
lithsemia  or,  as  the  older  writers  put  it,  rheumatism  or  gout  of  the 
brain.  Digestive  disturbances,  worms,  dentition,  hereditary  syphilis, 
mental  strain,  fright,  and  excitement  are  placed  among  the  causes. 
It  sometimes  appears  to  be  a  paroxymal  neurosis  allied  to  epilepsy 
and  some  cases  are  really  epileptic.  The  disorder  is  usually  harmless 
and  the  prognosis  favorable. 

Somnolentia,  or  sleep-drunkenness,  is  a  condition  of  incomplete  sleep 
in  which  a  part  of  the  faculties  is  abnormally  excited  while  the  other 
is  buried  in  repose.  It  is  a  kind  of  acted  nightmare  or  somnambulic 
delirium.  The  person  affected,  is  incoherent,  excited,  and  often  violent. 
He  experiences  the  delusion  of  some  impending  danger,  and  while  under 
it  acts  of  violence  have  been  committed.  A  patient  of  mine  was  in  the 
habit  of  waking  and  attacking  his  beloved  wife.  The  condition  is  one 
of  medico-legal  importance,  therefore,  and  has  been  discussed  by  writers 
on  that  science  (Wharton  and  Stille).  Minor  degrees  of  it  are  often 
noticed  in  children  and  in  adults  who  are  roused  from  a  very  profound 
sleep.  It  at  times  becomes  a  habit  and  a  most  annoying  or  dangerous 
one.     The  disorder  in  its  severe  form- is  fortunately  very  rare. 

The  treatment  of  morbid  dreams,  nightmare,  and  pavor  nocturnus 
must  be  directed  to  a  removal  of  the  causes.  Tonics,  cardiac  stimu- 
lants, laxatives,  antirheumatics,  attention  to  diet  and  time  of  eating 
are  especially  important.  Change  in  surroundings  is  often  necessary. 
Among  symptomatic  remedies  the  bromides  are  the  best,  combined 
sometimes  with  alkalies  and  salicylates.  In  somnolentia  the  patient 
should  be  prevented  from  getting  into  too  profound  sleep.     He  may  be 


592  DISEASES    OF    THE    NEEVOUS    SYSTEM 

awakened  once  or  twice  during  the  night,  or  take  a  nap  in  the  day- 
time. The  head  in  sleeping  should  be  raised  and  the  body  not  too 
heavily  covered. 

Somnambulism. — Somnambulism  is  a  condition  similar  to  hypno- 
tism or  the  mesmeric  state.  In  it  volition  is  abolished  and  the  mind 
acts  automatically  under  the  dominance  of  some  single  idea.  It  is  an 
acted  dream.  Sight,  hearing,  and  nearly  all  the  avenues  of  sense  are 
closed.  The  sleepwalker  avoids  obstacles  and  performs  ordinary 
acts  automatically  like  an  absent-minded  man,  which  in  reality  he  is. 
All  those  mechanisms  which  have  been  trained  by  constant  repetition 
to  act  automatically  like  that  which  preserves  equilibrium  are  active, 
and  their  powers  may  even  be  heightened,  so  that  the  somnambulist 
may  walk  along  roofs  or  on  dangerous  roads  and  thread  intricate  passages 
without  harm.  The  automatism  of  the  somnambulist  may  continue  for 
hours,  until  a  journey  has  been  performed  or  a  task  completed.  He  may 
carry  out  with  success  familiar  mathematical  calculations,  write  a  letter, 
or  work  upon  a  picture,  but  he  only  follows  along  the  lines  established  by 
constant  iteration  in  his  waking  moments.  He  can  originate  nothing  new. 
He  is  roused  from  his  state  with  difficulty,  and  when  out  of  it  he  re- 
members nothing  of  what  has  occurred. 

Somnambulism  occurs  oftener  in  neuropathic  persons  and  it  may  be 
hereditary.  Its  exciting  cause  is  often  over-eating,  or  mental  strain  and 
excitement.  Sleeping  with  the  head  too  low  is  another  cause.  The 
habit  being  once  established,  however,  attacks  occur  without  apparent 
cause.  The  disorder  occurs  oftenest  in  young  people  about  the  age  of 
puberty,  and  it  then  attacks  the  sexes  alike.  Later  in  life  women  are  more 
often  affected.  The  disease  is  fostered  sometimes  at  school  by  the  at- 
tentions of  the  schoolmates.  The  attacks  are  likely,  after  a  time,  to 
become  periodical,  occurring  every  week,  fortnight,  or  month.  The  som- 
nambulic state  may  come  upon  a  person  in  the  daytime.  It  is  then  re- 
garded as  spontaneous  trance,  or  hypnotism.  It  is  not  the  case,  however, 
that  persons  who  are  easily  hypnotized  are  usually  somnambulists,  though 
the  reverse  may  be  true.  Somnambulism  is  a  term  that  should  include 
not  only  sleep  walking,  but  sleep  talking. 

In  the  treatment  of  somnambulism  the  patient's  surroundings  must 
be  investigated,  and  unfavorable  influences,  such  as  excessive  fatigue  and 
excitement  and  such  as  may  occur  at  school  or  from  injudicious  nurses,  be 
removed.  He  should  be  prevented  from  sleeping  too  soundly,  the  head 
should  be  raised,  the  clothing  light,  the  diet  regulated.  Remedies  like 
iron,  quinine,  phosphorus,  and  cod-liver  oil  may  be  given.  When  the 
patient  is  discovered  in  the  somnambulistic  state  he  should  not  be 
awakened,  or  at  least  not  until  he  is  safely  back  in  bed. 


THE    DISORDERS    OF    SLEEP  593 

HYPNOTISM,   TRANCE,   MESMERISM 

Major  hypnotism  is  a  morbid  mental  state  artificially  produced  and 
characterized  by  (1)  perversion  or  suspension  of  normal  consciousness; 
(2)  abeyance  of  volition;  (3)  a  condition  of  suggestibility  leading  the 
patient  to  yield  readily  to  commands  or  external  sense  impressions ;  and 
(4)  intense  narrowing  and  concentration  of  the  attention  upon  some  idea 
or  feeling  suggested  by  the  hypnotizer. 

Minor  hypnotism  is  a  state  closely  bordering  on  normal  sleep  in 
which  there  is  a  dulling  of  consciousness  and  a  condition  of  suggesti- 
bility and  narrowing  of  the  attention  field.  ^ 

The  proportion  of  persons  of  all  ages  found  by  Beannis  to  be  hyp- 
notizable  was  about  eighteen  or  twenty  per  hundred.  Children  up  to 
the  age  of  fourteen  are  very  susceptible.  After  the  age  of  fifty-five 
susceptibility  lessens.  Men  are  almost  as  easily  affected  as  women; 
but  persons  of  a  docile  mind  and  those  trained  to  some  degree  of  mental 
discipline  and  capacity  for  submission,  such  as  soldiers  and  artisans,  are 
more  sensitive.  In  this  country  the  percentage  of  hypnotizable  sub- 
jects is  less  than  it  is  in  Europe.  Hysterical  and  insane  persons  are 
not  very  susceptible.  Those  who  have  been  mesmerized  once  are  more 
easily  affected  afterward,  and  may  even  pass  into  the  state  involuntarily. 

Methods. — -There  are  two  ways  of  inducing  hypnotism:  the  fixation 
method  and  the  suggestive  method.  The  former  and  older  plan,  de- 
vised by  Braid,  is  to  make  the  patient  fix  his  eyes  for  five  to  ten  minutes 
on  some  bright  object  at  a  distance  of  six  or  eight  inches  from  the  eyes 
and  a  little  above  the  horizontal  plane  of  vision.  Practically,  it  is  some- 
times the  custom  among  practising  hypnotizers  to  give  the  patient  a 
dose  of  paraldehyde. 

In  the  ''suggestive  method"  devised  by  Liebault  and  Bernheim 
the  subject  is  placed  in  a  chair  in  front  of  the  operator.  The  operator 
then  talks  to  the  subject  in  a  firm  and  confident  voice,  assuring  him 
that  he  will  go  to  sleep  in  a  short  time,  telling  him  to  make  no  resist- 
ance, that  his  sleeping  will  be  natural,  that  nothing  will  be  done  to  worry 
or  fatigue  him,  that  he  will  dream  pleasant  dreams,  that  he  will  wake  up 
feeling  better;  then  that  he  is  feeling  drowsy,  his  eyes  are  heavy,  objects 
look  confused,  the  lids  are  falling,  they  are  closed — ^in  a  moment  more 
the  patient  goes  off  to  sleep.  This  requires  some  little  time — five  to 
fifteen  minutes.     It  may  fail  the  first  time  and  succeed  the  second. 

Hypnotic  states  can  be  self-induced  by  vigorously  fixing  the  atten- 
tion upon  some  object.     The  ecstatic  states  of  the  saints  are  forms  of 

"•The   definitions  of  hypnotism  vary  with  the  psychologists  and  the  time  of  year. 
The  above  is  only  a  descriptive  definition  with  no  reference  to  dissociations  of 
personality  or  the  thresholds  of  consciousness.     1  may  add  that  the  word  hypnotism 
is  used  in  two  senses.     It  indicates  a  mental  state  and  a  general  topic. 
38 


594  DISEASES    OF    THE    NERVOUS    SYSTEM 

hypnotism;  so  also  are  the  trance  states  in  which  some  clairvoyants  and 
spiritualistic  preachers  place  themselves;  this  same  curious  phenomenon 
is  at  the  bottom  of  the  "mind-healing"  sciences,  and  it  enters  into 
rational  therapeutics  and  orthodox  religion.  The  capacity  of  the  human 
mind  for  hypnotism  or  semihypnotic  states  is,  therefore,  a  most  curious 
and  important  fact. 

Symptoms. — The  person  who  has  been  hypnotized  at  first  sits  or  lies 
quietly  in  the  position  he  has  assumed  during  the  manipulations  of  the 
operator.  No  notable  physiological  changes  occur,  as,  for  example,  in 
the  pulse,  respiration,  temperature,  pupils,  skin,  etc.  Some  increase  in 
the  cerebral  blood-supply,  however,  is  said  to  be  present.  The  patient 
will  now  respond  automatically  to  any  outside  command  or  will  be  dom- 
inated by  any  idea  which  is  suggested  to  him.  He  will  talk,  or  walk, 
or  run,  or  gesticulate,  assume  expressions  of  fright,  anger,  or  joy,  entirely 
in  accordance  with  the  command  given.  Apart  from  these  commands, 
he  is  entirely  dead  to  the  outside  world.  He  hears,  sees,  smells,  tastes, 
and  feels  nothing.  He  can  be  burned,  cut,  or  injured  without  showing 
any  signs  of  feeling.  At  a  suggestion  he  may  be  made  cataleptic, 
somnambulic,  or  paralytic.  This  state  is  termed  somnmnbulistic  trance. 
If  left  to  himself,  he  gradually  sinks  into  a  deep  sleep,  from  which  he  can 
with  difficulty  be  roused.  After  a  time,  rarely  more  than  one  or  two 
hours,  he  awakes  as  from  ordinary  slumber.  This  latter  state  is  called 
trance  coma,  or  lethargic  hypnotism. 

The  phenomena  of  hypnotism  depend  upon  the  wonderful  sensi- 
tiveness and  quickness  of  the  subject  in  responding  involuntarily,  with 
all  his  nervous  energy,  to  outside  suggestion.  Dishonest  persons  may 
learn  the  latter  trick  and  thus  simulate  the  hypnotic  state.  Traveling 
mesmerizers  utilize  such  persons  largely;  hence  no  confidence  can  be 
placed  in  the  phenomena  exhibited  by  them. 

Minor  hypnotism  is  produced  by  the  ''suggestive  method"  of  hyp- 
notizing. By  this  latter  plan  patients  are  thrown  into  various  degrees 
of  the  hypnotic  state  from  slight  drowsiness  to  lethargy,  but  they  are 
not  somnambulic,  and  do  not  become  cataleptic  or  ansesthetic. 

Patients  naturally  come  out  of  the  mesmeric  state  through  the  channel 
of  deep  sleep  or  lethargy.  Ordinarily  they  are  dehypnotized  by  word 
of  command,  or  by  a  pass  of  the  hand,  or  any  impression  which  the  patient 
expects  to  be  used  for  the  purpose. 

Hypnotized  persons  have  been  observed  to  have  a  diminution  in  the 
spinal  reflexes  and  a  muscular  hyperexcitability.  They  sometimes  show 
a  most  extraordinary  exaltation  of  visual,  auditory,  or  other  special  sense. 

Therapeutics. — The  practice  of  using  major  hypnotization  is  usually 
injurious,  if  repeated  much,  tending  to  exhaust  the  nervous  force  and 
weaken  the  will.     It  should  be  done  only  with  the  greatest  care.     Its 


THE    DISORDERS    OF    SLEEP  595 

utility  in  therapeutics  I  greatly  doubt.  It  may  relieve  symptoms  in  the 
hysterical  for  a  time,  but  it  cannot  be  of  permanent  benefit  and  is  likely 
to  lead  to  actual  harm. 

The  induction  of  minor  hypnotic  states  by  suggestion  is  not  harmful 
if  carefully  and  moderately  employed.  Its  practical  results,  however, 
are  not  great.  It  has  its  value  in  pedagogy,  among  children,  in  defec- 
tives, obsessives,  and  in  morbid  habits.  The  general  popularization  of 
hypnotism  by  means  of  mind  cures.  Christian  science,  etc.,  accomplishes 
its  results  at  the  expense  of  mental  demoralization,  and  faith-healing 
institutes  may  be  pernicious  elements  in  society. 

MORBID  DROWSINESS  AND  SOMNOLENCE 

This  is  a  common  symptom,  which  may  be  due  to  one  or  more  of 
he  following  causes:  1.  Old  age  when  there  is  a  weakened  heart  and 
cerebral  arterial  sclerosis.  2.  Cerebral  syphilis.  3.  Endogenous  toxae- 
mias such  as  result  from  constipation,  gastric  repletion,  atonic  intestines, 
and  the  metabolic  disturbances  in  obesity.  4.  Concussion  of  the  brain. 
5.  Disorder  of  the  pituitary  or  thyroid  glands.  6.  Climatic  conditions 
such  as  extreme  cold.     7.  Constitutional  defects. 

A  very  common  cause  of  drowsiness  is  dyspepsia  attended  by  some 
torpidity  of  the  liver,  the  condition  popularly  known  as  "biliousness." 
Syphilis  is  more  likely  to  cause  insomnia,  but  in  its  parenchymatous  form 
somnolent  conditions  may  be  produced  which  are  of  serious  significance. 
Drowsiness  occurs  from  the  effects  of  severe  cold.  It  sometimes  develops 
when  persons  change  their  surroundings,  especially  on  going  to  the  sea- 
shore, for  low  levels  and  a  high  degree  of  atmospheric  pressure  seem  to 
promote  sleep.  The  drowsy  state  that  sometimes  follows  concussion  of 
the  brain  is  a  familiar  phenomenon.  Some  persons,  no  doubt,  acquire 
the  habit  of  drowsiness.  At  first  the  trouble  may  have  been  induced  by 
indigestion,  "biliousness,"  or  malarial  infection,  but  it  persists  after  the 
cause  is  removed.  Such  persons  can  hardly  sit  through  a  lecture,  a  church 
service,  or  any  exercise  requiring  quiet  and  attention.  Morbid  somno- 
lence is  sometimes  produced  by  disordered  activity  of  the  pituitary  and 
thyroid  glands.  The  patients  are  unable  to  keep  awake  except  when 
actively  engaged  in  work.  Sitting  at  a  table  or  in  the  chair  they  fall 
asleep  and  sleep  so  profoundly  that  they  fall  to  the  floor. 

Morbidly  Deep  Sleep. — Certain  persons,  when  they  sleep,  pass  into 
an  almost  lethargic  slumber.  Persons  who  suffer  in  this  way  often  sleep 
a  longer  time  than  normal.  They  are  awakened  with  difficulty  and  then 
suffer  with  headache  or  disagreeable  sensations  throughout  the  day. 
Instances  in  which  persons  retire  at  the  usual  hour,  but  can  with  great 
difficulty  be  roused  in  time  for  the  ordinary  duties  of  the  day,  are  not 


596  DISEASES    OF    THE    NERVOUS    SYSTEM 

rare.  Some  of  these  are  illustrations  of  the  vice  of  indolence,  but  in  other 
cases  there  is  an  absolute  need  of  nine,  ten,  or  even  fourteen  hours  of  sleep. 

This  disorder  of  sleep  is  most  liable  to  occur  in  the  young  and  in  those 
of  nervous  temperament.  It  often  seems  to  be  a  constitutional  condi- 
tion, for  which  nothing  can  be  done.  In  other  cases  it  results  from 
over-feeding  and  indolent  habits. 

Paroxysmal  Sleep,  Narcolepsy,  Sleep  Epilepsy. — It  sometimes  hap- 
pens that  persons  suffer  from  sudden  attacks  of  unconquerable  drowsi- 
ness; they  fall  off  into  slumber  despite  every  effort  of  the  will.  These  are 
more  than  drowsy  sensations,  for  sleep,  or  a  state  resembling  it,  cannot  be 
kept  off.  Some  of  these  cases  are  of  a  purely  nervous  character,  i.e.,  the 
trouble  is  not  due  to  a  toxsemia  or  to  organic  disease,  but  to  a  parox- 
ysmal change  in  the  nervous  centres  of  a  vascular  or  chemical  character, 
causing  sleep.  It  may  be  that  the  patient  is  epileptic  and  sleep  seizure 
takes  the  place  of  the  ordinary  epileptic  spasms. 


Fig.  255. 

Cases  of  epileptic  sleep,  or  narcolepsy,  and  allied  forms  are  not  of 
frequent  occurrence.  Females  are  rather  more  often  affected  than  males, 
and  the  susceptible  age  is  from  fifteen  to  forty.  The  disorder  is  brought 
on  sometimes  by  fright,  over-strain,  and  humoral  poisons  acting  on  a  pre- 
disposed nervous  system. 

The  course  is  chronic  and  relief  is  not  always  obtained.  It  should 
be  remembered  that  syphilis,  malaria,  or  ansemia,  and  indigestion  may  be 
elements  in  the  trouble  which  are  important,  if  not  fundamental.  Bro- 
mides in  small  doses  are  often  useful  factors  in  treatment.  Change  of 
occupation,  of  mode  of  life,  or  of  climate  may  be  essential  to  a  cure. 

Catalepsy,  Trance.^ — Most  of  the  so-called  cases  of  prolonged  sleep, 
lasting  for  days  or  weeks,  are  cases  of  spontaneously  developed  mes- 
meric sleep  in  hysterical  women,  or  cases  of  incipient  insanity  (dementia 


THE    DISORDEES    OF    SLEEP  597 

prsecox  or  stuporous  melancholia).  The  phenomena  in  these  cases  may 
take  the  form  of  catalepsy,  with  waxy  rigidity  of  the  limbs,  or  of  a  trance 
state.  In  cataleptic  states  the  limbs  may  be  placed  in  various  posi- 
tions and  will  remain  there  for  several  minutes  (Fig.  255).  In  lethargy 
or  trance  states  the  patient  may  be  plunged  into  a  deep  and  prolonged 
unconsciousness,  lasting  from  one  day  to  several  years.  These  are  the 
''sleeping  girls"  of  the  newspapers.  Others  are  persons  of  a  too  ready 
susceptibility  to  mesmeric  suggestion,  who  get  into  a  morbid  habit  of 
going  into  mesmeric  sleep  spontaneously. 

The  duration  of  the  attacks  of  trance  lethargy  is  from  a  few  hours 
to  ten  years.  Ordinarily,  however,  profound  trance  sleep  lasts  not 
more  than  a  few  days,  while  those  cases  in  which  the  sleep  is  from  mes- 
meric suggestion  lasts  but  a  few  hours. 

The  katatonic  patients  after  a  few  weeks  or  months  gradually  awake, 
become  excited,  and  then  pass  into  a  condition  of  dementia  or  into  cata- 
lepsy again. 

Morbid  Sleep  from  Organic  Disease. — Prolonged  and  excessive  sleep 
occurs  as  the  result  of  syphilis  of  the  brain,  brain  tumors,  and  the  degen- 
erative changes  in  old  age  and  insanity.  It  has  been  noted  especially 
in  tumors  of  the  basal  ganglia  and  third  ventricle. 

Organic  diseases  of  the  brain  tend  to  produce  conditions  of  mental 
weakness,  hebetude,  or  comatose  states,  rather  than  anything  allied  to 
sleep. 

Accidents  of  Sleep. — Owing  to  the  fact  that  sleep  is  a  resting  state 
of  the  organism,  and  that  many  of  its  functions  are  lowered,  or  their 
cerebral  control  lessened,  peculiar  crises,  or  physiological  and  pathological 
disturbances  of  nervous  equilibrium,  occur.  Attacks  of  gout,  of  asthma, 
and  of  pulmonary  hemorrhage  are  most  liable  to  occur  during  the  early 
morning  hours.  Deaths  and  suicides  occur  oftener  in  the  forenoon,  but 
births  oftener  at  night.  Epileptic  and  eclamptic  attacks  occur  with 
much  frequency  at  night.  Involuntary  emissions  of  spermatic  fluid,  or 
gastric  crises,  and  incontinence  of  urine  are  among  the  pathological  inci- 
dents of  sleep. 

Praedormitial  Shocks. — Sudden  attacks  of  starting  of  the  whole  body, 
shock-like  in  character,  accompanied  by  peculiar  feeling  in  the  head  or 
occiput,  not  infrequently  attack  persons  as  they  are  dropping  off  to  sleep. 
They  indicate  fatigue  and  are  of  slight  significance. 

THE  SLEEPING  SICKNESS  OF  AFRICA 

The  sleeping  sickness  of  Africa  is  a  disease,  caused  by  a  species  of 
flagellated  protozoa,  belonging  to  the  genus  Trypanosoma.  This  para- 
site multiplies  in  the  blood,  and  causes  a  slowly  developing  malady  char- 


598 


DISEASES    OF    THE    NERVOUS    SYSTEM 


acterized  by  somnolence,  mental  apathy,  paralysis,  and  finally  death. 
The  Trypanosome  which  causes  this  sleeping  sickness  is  the  T.  Gainhiense, 
first  described  by  Dr.  J.  E.  Dutton. 

Etiology. — -The  disease  prevails  mostly  along  the  west  coast  of  Africa, 
but  it  has  extended,  thence,  to  other  parts  of  that  continent,  particu- 
larly equatorial  Africa.  It  was  formerly  confined  to  the  negroes,  but 
recently  Europeans  have  suffered  from  it.  It  affects  particularly  natives 
who  live  upon  the  shore  of  the  rivers  and  lakes.  The  Trypanosome  is  a 
worm-like  parasite  which  is  found  among  the  red  blood-cells  (Fig.  256). 
They  are  not  very  numerous,  and  several  microscopical  examinations 
may  be  needed  to  find  them.  In  late  stages  of  the  disease,  the  parasite 
is  found  in  the  cerebrospinal  fluid,  while  early  in  the  stage  it  is  found  in 
the  lymphatic  glands  and  channels.     The  common  way  of  the  propaga- 


FiG.  256. — The  blood  in  sleeping  sickness,   showing  spirillum. 

tion  of  the  Trypanosome  is  through  the  tsetse-fly,  and  it  is  conveyed 
back  to  man  by  the  bites  of  these  flies. 

Symptoms. — ^It  is  stated  by  Dr.  David  Bruce  that  after  the  Trypano- 
some has  infected  the  body,  it  may  be  from  three  months  to  three  years 
before  it  gets  into  the  cerebrospinal  fluid,  and  begins  to  produce  definite 
symptoms.  During  this  stage  of  incubation,  there  is  some  enlargement 
of  the  lymphatic  glands,  and  sometimes  a  fever  of  irregular  type.  When 
the  disease  begins  to  affect  the  patient,  he  becomes  apathetic  and  dis- 
inclined to  exert  himself.  Headache  and  indefinite  pains  are  complained 
of.     The  pulse  is  rapid  and  weak.     The  cervical  and  other  lymphatic 


THE    DISOEDERS    OF    SLEEP  599 

glands  are  enlarged,  the  gait  is  unsteady  and  shuffling,  the  muscular 
powers  diminished,  the  voice  is  weak,  and  tremors  of  the  tongue  are 
noted.  The  symptoms  increase  until  after  weeks  or  months  the  patient 
is  confined  to  his  bed,  lying  in  a  somnolent  condition.  The  patient  then 
begins  to  emaciate,  becomes  semicomatose,  and  in  two  or  three  weeks 
the  temperature  falls  and  death  occurs. 

Pathology. — Dr.  F.  V.  Mott  has  shown  that  there  is  a  characteristic 
appearance  in  sections  of  the  brain,  which  is  found  in  no  other  disease. 
This  is  a  condition  of  meningo-encephalo  myelitis,  which  affects  especially 
the  medulla  and  the  base  of  the  brain.  The  inflammation  can  be  traced 
along  the  blood-vessels  into  the  substance  of  the  nervous  system,  the 
perivascular  lymphatics  being  crowded  with  lymphocytes.  Modern 
trypanosomiasis  is,  however,  according  to  Bruce,  a  disease  of  the  lym- 
phatic system,  though  its  characteristic  symptoms  are  shown  upon  the 
nerves  and  muscular  system. 

Diagnosis. — The  diagnosis  is  difficult  in  the  early  stage  of  the  disease. 
Later,  the  examination  of  the  blood  and  lymphatics,  and  the  peculiar 
progressive  weakness  of  the  body,  tremor  of  the  muscles,  unsteady  gait 
and  somnolence  are  characteristic. 

Pro gno sis. ^^E very  case  of  the  disease  dies  sooner  or  later,  according 
to  Dr.  Bruce. 

Treatment. — Up  to  the  present  time  the  most  effective  drug  has  been 
some  preparation  of  arsenic.  The  prophylactic  measure  for  the  sleep- 
ing sickness  is  to  kill  off  the  tsetse-fly. 


CHAPTER  XXX 
CRANIO -CEREBRAL  TOPOGRAPHY 

The  object  of  cranio-cerebral  topography  is  to  map  out  upon  the 
scalp  the  underlying  fissures,  convolutions,  and  other  parts  of  the  brain. 
Practically,  the  principal  points  to  be  determined  are  the  position  of  the 
longitudinal,  Rolandic,  Sylvian,  and  parieto-occipital  fissures  and  the 
lower  outline  of  the  brain. 

The  measurements  are  based  chiefly  upon  the  known  relations  of 
certain  landmarks  on  the  skull  to  the  parts  beneath.  These  landmarks 
are  the  glabella,  bregma,  lambda,  stephanion,  asterion,  and  pterion,  which 
are  points  at  the  junction  of  the  various  sutures  with  each  other  and  with 
certain  ridges  or  protuberances.  Their  position  is  shown  in  the  cut  (Fig. 
252)  except  that  of  the  glabella  or  prominence  just  above  the  nasofrontal 
suture.     The  inion  is  identical  with  the  occipital  protuberance. 

The  following  rules  are  based  upon  the  observations  of  Heftier,  Thane, 
R,eid,  Horsley,  Fraser,  and  myself: 

I.  The  longitudinal  fissure.  This  corresponds  with  the  naso-occipital 
arc. 

II.  The  fissure  of  Rolando.  Measure  the  distance  from  the  glabella 
to  the  inion;  find  55.7  per  cent,  of  this  distance,  and  the  figures  obtained 
will  indicate  the  distance  of  the  upper  end  of  the  fissure  of  Rolando  from 
the  glabella.  It  should  be  about  48  mm.  behind  the  bregma  in  male 
adults,  45  mm.  in  women,  30  to  42  mm.  in  infants  and  young  children, 
respectively. 

The  fissure  runs  downward  and  forward  for  a  distance  of  about  10 
cm.  measured  on  the  scalp,  the  real  length  being  about  8.5  cm.  The 
fissure  makes  an  angle  of  about  67°  with  the  anterior  part  of  the  longi- 
tudinal fissure.  The  lower  third  of  it  is  more  vertical,  and  the  lower  end 
is  25  to  30  mm.  behind  the  coronal  suture.  The  fissure  is  shorter  in 
children. 

III.  The  fissure  of  Sylvius  runs  nearly  horizontally,  and  lies  either 
under  or  a  little  above  the  uppermost  part  of  the  parieto-squamous  suture. 
This  suture,  the  external  orbital  process,  and  the  parietal  eminence  are  the 
guiding  landmarks  by  help  of  which  the  surgeon  can  often  operate  with- 
out marking  down  lines  on  the  scalp.  In  children  the  fissure  is  sometimes 
higher  and  more  oblique.  n 

Reid's  method  of  finding  the  fissure  of  Sylvius  is  to  ''draw  a  line  from 

600 


CRANIO-CEREBRAL    TOPOGRAPHY 


601 


a  point  134  inches  behind  the  external  angular  process  to  a  point  %  inch 
below  the  parietal  eminence.  The  ascending  branch  starts  from  a  point 
%  inch  back  from  the  anterior  end  of  this  line,  and  2  inches  (5  cm.)  back 
of  the  external  angular  process." 

IV.  To  outline  the  parieto-occipital  fissure,  find  the  lambda,  mark  a 
point  3  mm.  anterior  to  it,  draw  a  line  through  this  at  right  angles  to 
the  longitudinal  fissure,  extending  about  2.5  cm.  (1  inch)  on  each  side 
of  the  median  line.  This  marks  the  position  of  the  fissure.  If  the  lambda 
cannot  be  felt,  its  position  may  be  found  by  measuring  the  naso-occipital 
arc  and  taking  22.8  per  cent,  of  it.  This  indicates  the  distance  of  the 
lambda  from  the  inion  or  external  occipital  protuberance.     The  average 


Fig. 


257. — Showing  the  position  of  the  bony  points  on  the  cranium,  the  sutures,  and 
the  principal  underlying  fissures,  also  the  basal  outline  of  the  brain. 


distance  in  male  adults  is  7.42  cm.  (2%  inches).     It  is  greater  in  women 
than  in  men  by  a  little  over  a  millimetre. 

V.  To  outline  the  frontal  lobes:  The  anterior  end  of  the  frontal  lobes 
reaches  to  a  point  determined  by  the  thickness  of  the  frontal  bone.  This 
ranges  from  2  to  8  or  more  mm.  (3^2  to  3^  inch).  The  floor  of  the  anterior 
fossa  reaches  in  front  to  a  level  a  little  above  the  supra-orbital  margin 
(16  mm.,  %  inch — Heftier).  It  slopes  down  and  backward,  its  pos- 
terior limit  being  indicated  by  the  lower  end  of  the  coronal  suture. 

VI.  To  outline  the  temporal  lobe  and  the  lower  border  of  the  cere- 
brum: The  temporal  lobe  is  limited  above  by  the  fissure  of  Sylvius,  below 
by  the  contour  line  of  the  lower  border  of  the  cerebrum.  This  latter  cor- 
responds to  a  line  drawn  from  a  point  slightly  (about  12  mm.)  above  the 
zygoma  and  the  external  auditory  meatus  to  the  asterion,  and  continued 


602 


DISEASES    OF    THE    NERVOUS    SYSTEM 


on  along  the  superior  occipital  curve  to  the  inion.  The  anterior  border 
of  the  lobe  corresponds  to  the  posterior  border  of  the  orbital  process  of  the 
malar  bone. 

The  temporal  lobe  is  about  4  cm.  (1%  inches)  wide  at  the  external 
auditory  meatus.  A  trephine,  as  Bergmann  states,  placed  half  an  inch 
above  the  meatus  would  enter  the  lower  part  of  the  lobe.  The  middle 
of  the  lobe  is  in  a  vertical  line  from  the  posterior  border  of  the  mastoid 
process.  A  line  from  the  upper  end  of  the  fissure  of  Rolando  to  the  point 
of  the  process  would  pass  through  this  important  sensory  area  (Fig.  259). 


Lambda 


Inion 


Fig.  258. — Showing  anatomical  landmarks  on  skull. 


VII.  To  find  the  position  of  the  central  ganglia,  viz.,  corpus  striatum 
and  optic  thalamus,  draw  a  line  from  the  upper  end  of  the  fissure  of 
Rolando  to  the  asterion,  practically  a  vertical  line.  This  limits  the  optic 
thalamus  posteriorly.  A  vertical  line  parallel  to  the  first,  a  little  in  front 
of  the  beginning  of  the  fissure  of  Sylvius,  limits  the  corpus  striatum 
anteriorly.  A  horizontal  plane  45  mm.  (1%  inches)  below  the  surface 
of  the  scalp  at  the  bregma  limits  the  ganglia  superiorly.  The  ganglia 
lie  about  35  mm.  (13^  inches)  below^the  superior  convex  surface  of  the 
brain  (Fere). 

VIII.  To  reach  the  lateral  ventricles:  A  number  of  routes  may  be 


NERVOUS  DISEASES 

Dana 


PLATE  IV 


Composite  Photograph  Showing  Relations  op  Cranial  Surface  to 
THE  Fissures  and  Convolutions.     {Alec  Fraser.) 


CEANIO-CEREBRAL    TOPOGRAPHY  603 

taken.  The  lateral  is  recommended  by  Keen.  Mark  a  point  13-^  inches 
behind  the  external  auditory  meatus  and  13^^  inches  above  a  base  line 
made  by  drawing  a  line  through  the  lower  border  of  the  orbit  and  the 
external  auditory  meatus.  Trephine  at  this  point  and  plunge  the  director 
into  the  brain  in  the  direction  of  a  point  23^^  to  3  inches  vertically  above 
the  opposite  external  meatus.  The  ventricle  lies  at  a  depth  of  2  to  23^ 
inches  (5  to  5.7  cm.). 

Mr.  Alec  Eraser  has  devised  a  way  of  mapping  out  the  fissures  by 
means  of  a  series  of  composite  photographs,  so  taken  as  to  show  the  rela- 
tion of  the  underlying  parts  to  certain  tapes  tacked  upon  the  skull.  One 
of  his  figures  is  reproduced  here  (Plate  IV). 

In  applying  this  method  the  surgeon  tacks  the  tapes  on  the  shaved 
scalp.  Then  looking  at  the  diagram,  he  finds  where  the  point  in  the 
brain  is  that  he  wishes  to  reach  and  notes  its  relation  to  the  median 
lateral  circumferential  tapes.  Then  as  the  circumference  of  the  illus- 
trated head  is  to  the  circumference  of  the  living  one,  so  is  the  position  of 
the  area  on  the  tapes  in  the  illustrated  head  to  the  desired  position  of 
the  same  area  in  the  living  one.  The  illustration  is  a  composite  of  several 
adult  heads  varying  in  circumference  from  203-^  to  233^2  inches. 

The  cranial  measurements  necessary  to  indicate  the  location  of  the 
important  fissures  and  convolutions  are  given  above.  There  are  a  num- 
ber of  other  methods,  but  no  very  important  improvements  upon  the 
original  one  of  Reid.  I  have  repeatedly  verified  the  methods  given  and 
see  no  reason  to  change  them.  Some  surgeons,  however,  prefer  the  Ander- 
son-Makin  method.  According  to  this,  the  upper  end  of  the  fissure  of 
Rolando  corresponds  to  a  point  one-half  to  three-quarters  of  an  inch 
behind  the  mid-point  between  the  inion  and  glabella.  The  upper  ex- 
tremity of  the  parieto-occipital  fissure  corresponds  to  a  point  one- 
quarter  of  an  inch  behind  the  mid-point  between  the  line  of  the 
Rolandic  fissure  and  the  inion. 

As  surgical  approach  to  brain  tumors  is  now  done  by  large  bone 
flaps,  Dr.  Charles  K.  Mills  has  outlined  the  various  areas  to  be  attacked, 
corresponding  to  the  pre-frontal,  post-frontal,  parieto-temporal,  mid- 
frontal,  parietal  and  occipital  areas.  Having  determined  the  location 
of  the  Rolandic,  Sylvian  and  parieto-occipital  fissures,  the  location  of 
these  flaps  is  easily  determined. 


APPENDIX 

THE  FUNCTION  AND  INNERVATION  OF 
THE  MUSCLES 


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APPENDIX 
Muscles  of  Back  and  Lower  Extremities 


Name  of   Muscle 


Innervated  by 


Symptoms  of  Deficient  Action 


Erector  spinse;  sacro-lumbalis 
longissimus  dorsi. 


Abdominal  muscles. 

Quadratus  lumborum. 
Adductor  muscles. 
Sartorius. 
Quadriceps  femoris. 

Ilio-psoas. 

Tensor  fascise  latae. 

External  rotators: 

Pyriformis  I 

Gemelli  j 

Quadratus  femoris.  ! 

Internal  obturator.  | 

External  obturator.  J 

Gluteal  muscles. 


Biceps:    semitendinosus    and 
semimembransous. 


Gastrocnemius    (also   planta- 

rius  and  soleus). 
Anterior        tibial         muscles 

(tibialis     anticus,     extensor 

digitorum,      and      extensor 

pollicis  longus). 

Peroneus  longus. 


Posterior  tibial  muscle 


Peroneus  brevis. 

Interossei      pedis      et      lum- 
bricales. 


Adductor;    flexor   brevis   and 
abductor  hallucis. 


Dorsal     nerves.     Second     to 
twelfth  dorsal  segments. 


Dorsal     nerves.     Second     to 
twelfth  dorsal. 


Lumbar  nerves. 

Obturator  nerve,  great  sciatic 
and  crural. 

Crural.  Third  lumbar  seg- 
ment. 

Crural.     Third  lumbar. 


Crural        (lumbar        plexus). 

Fourth  lumbar. 
Superior         gluteal.     Fourth 

lumbar. 

Sacral     plexus  (muscular 

branches').     Fifth  lumbar. 

Obturator  nerve  (lumbar 
plexus) . 

f  Inferior  gluteal  (sacral 
plexus) .     First  and  second 

'l    sacral. 

I  Gluteal  superior.     First  and 

I    second  sacral. 

Sciatic.  Fifth  lumbar  seg- 
ment. 


Internal  popliteal.     Fifth 

lumbar. 

Anterior  tibial.  Fifth  lum- 
bar and  first  sacral. 


Peroneal.     First   and   second 
sacral  segments. 

Posterior  tibial  nerve.     First 
and   second  segments. 

Peroneal.     First  and   second 

segments. 
Posterior    tibial.     First     and 

second  segments. 


Posterior    tibial.     First    and 
second  segments. 


Lordosis  of  lower  spine;  perpendicular 
line  from  shoulder  falls  behind  os  sac- 
rum; unilateral  palsy  causes  deflec- 
tion of  spine  toward  sound  side. 

Lordosis  with  protrusion  of  nates  and 
abdomen;  other  actions  deficient; 
cannot  straighten  up  from  recumbent 
position  without  assistance  of  hands. 

Lateral  movements  of  lower  vertebrse 
imperfect. 

No  adduction;  thigh  rolls  outward. 

Flexion  impaired;  acts  imperfectly. 

Leg  cannot  be  extended;  to  test  it  ask 
patient,    who   is   lying    down   with    hip 
bent,  to  stretch  out  the  leg;  when  pa- 
tient is  sitting  down  to  extend  leg. 
Flexion   difficult;   in   bed   thigh   cannot 

!    be    flexed;    difficulty  rising   from    the 

I    horizontal  position. 


Deficient    outward   rotation;    leg   turned 
inward. 


No  extension  of  thigh;  great  difficulty 
in  climbing;  no  abduction  of  thigh; 
waddling  gait,  exaggerated  movement 
of  plevis. 

Deficient  flexion;  action  of  quadriceps 
may  cause  excessive  extension;  in 
standing  thigh  is  flexed  to  excess;  trunk 
moved  backward. 

Deficient  flexion  of  foot;  heel  cannot 
be  raised;  cannot  stand  on  tiptoes. 

Deficient  extension;  "drop-foot,"  toes 
scrape  floor;  to  clear  this,  excessive 
flexion  at  knee  and  hip;  contracture 
of  flexors  and  pes  equinus  or  equino- 
varus. 

Deficient  abduction;  plantar  arch  les- 
sened; increased  by  contracture. 

1  Flatfoot;  walking  tiresome. 

1  Deflcient  abduction  or  adduction; 
!     deformities  result  from  deficiencies. 


Abduction  and  adduction  of  toes  defi- 
cient; paralysis  of  interossei;  hyper- 
extension  of  first  phalanges;  second 
and  third  flexed  (clawed  foot). 
Deficient  flexion  of  toes;  foot  cannot 
be  pushed  off  ground  easily. 


INDEX 


Abducens  nerve,  anatomy  of  the,  95 

paralysis  of  the,  102. 
Abscess,  cerebral,  395 
Acoustic  nerve,  anatomy  of  the,  171 

neuroses  of  the,  172 
Acrania,  374 
Acrodynia,  85 
Acromegaly,  578 
Acro-parsesthesia,  146 
Actinomycosis  of  the  brain,  467 
.^Esthesiometer,  55 
After-brain,  334,  335,  336 
Age  as  a  factor  in  the  etiology  of  nervous 

diseases,  24 
Ageusia,  179 
Agnosia,  37 
Agoraphobia,  508 
Agraphia,  369 
Akinesis,  34 
Alcohol    as  a  factor  in  the  etiology   of 

nervous  diseases,  26 
Alcoholism,  effect  of,  26 
Alexia,  368,  371 
Allochiria,  definition  of,  37 
Amaurosis,  157 
Amblyopia,  157 
Amimia,  370 
Amnesia,  tactile,  37 
Ampere,  definition  of,  65 
Amperemeter,  65 
Amputation  neuroma,  93 
Amusia,  370 
Amyelia,  216 

Amyotonia  congenita,  315 
Amyotrophic  lateral  sclerosis,  304 
Amyotrophy,  progressive  spinal,  293 

remitting  spinal,  243 
Ansemia,  cerebral,  393 

meningeal,  375 

of  nerves,  75 

pernicious,  combined   spinal  sclero- 
ses of,  282 
Anajsthesia,  definition  of,  35 

hysterical,  495 

muscular,  55 


Anaesthesia,  tests  for,  50 

trigeminal,  163 
Analgesia,  definition  of,  36 
Anarthria,  374 

Anatomy,  general,  of  the  nervous  sys- 
tem, 1 

of  the  brain,  333 

of  the  spinal  cord,  200 
Anencephaly,  374,  375 
Aneurisms,  intracranial,  473 

miliarjr,  of  the  brain,  473 
Angina  of  nerves,  75 
Angio-ataxia,  38 

-neurosis,  38 

-paralysis,  38 

-spasm,  38 
Angioneurotic     gangrene,     symmetrical, 
197 

oedema,  583 
Angiopathic  neurasthenia,  524 
Anidrosis,  definition  of,  38 
Ankle  clonus,  49 
Anomia,  369,  372 
Anorexia  nervosa,  502 
Anosmia,  151 
Aphasia,  368 

auditory,  369,  371 

clmical  types  of,  374 

conduction,  370,  374 

fronto-capsular,  371 
-lenticular,  373 

lenticular  zone,  373,  374 

mixed,  370,  373,  374 

motor,  370,  371 

occipital,  371 

optic,  372,  373 

parieto-occipital,  371 
-temporal,  371 

sensory,  370,  372 

subcortical,  371 

temporal,  372 

visual,  371 
Aphcmia,  369,  373 
Aphonia,  hysterical,  499 
Aphthongia,  124 


61; 


614 


INDEX 


Apoplexy,  cerebellar,  432 

cerebral,  424 

dural,  429 

embolic,  438 

hemorrhagic,  424 

medulla,  431 

meningeal,  429,  431 

pial,  431 

pons,  431 

spinal,  217,  218 

subdural,  430 

thalamus,  442 

thrombotic,  438 

vertebral,  431 
Apraxia,  368 
Arachnoid,  cerebral,  352 
Arbor  vita;  of  the  cerebellum,  344 
Arborization,  terminal,  6 
Arcades,  interfascicular,^  12 
Argyll-Robertson  pupil,  49 

in  locomotor  ataxia,  264 
Arm,  cord  centres  for  muscle  of  the,  610 

palsies  of  the,  133 

spasmodic  disorders  of  the,  133 
Arteries,  cerebral,  353,  356 

spinal,  210,  211,  213 
Arteriosclerosis  as  a  factor  in  the  etiology 

of  nervous  diseases,  27 
Arthritic  muscular  atrophy,  316 
Arthropathy    of   locomotor    ataxia,    266 
Articulation,  mechanism  of,  123 
Associated  movements,  34 
Association  centres  in  the  brain,  362 
Associative  functions  of  the  brain,  363 

neuron,  16 
Astereognosis,  36 
Asthenic  bulbar  paralysis,  302 

bulbospinal  paralysis,  302 
Asthenopia,  muscular,  103 
Astraphobia,  508 
Asymbolia,  37 
Asynergy,  56 
Ataxia,  cerebellar,  36,  56 

definition  of,  36 

family,  287 

Friedreich's,  286 

hereditary  cerebellar,  291 
spinal,  286 

locomotor,  257,   and   see  Locomotor 
ataxia. 

motor,  36,  257 
testing  for,  56 


Ataxia,  static,  36 

testing  for,  56 
tests  for,  56 
vestibular,  56 
Athetosis,  33 

Atrophia  musculorum  lipomatosa,  310 
Atrophies,  progressive  muscular,  292 
Atrophy,  arthritic  muscular,  316 

hereditary  muscular,  of  peroneal 

type,  298 
occupation  muscular,  317 
of  cervical  muscles,  129 
optic,  156 

progressive  muscular,  293 
facio-scapulo-humeral,  314 
hereditary,  298 

of  peroneal  type,  298 
spastic  form  of,  304 
spinal,  luetic  type  of,  297 
Auditory  nerve,  anatomy  of  the,  171 
neuroses  of  the,  171 
vertigo,  176 
Aura,  epileptic,  478 
Autonomic  nervous  system,  3 
Axis  cylinder,  5,  8,  9 
Axon,  5 

Babinski,  sign  of,  45 

Back,  cord  centres  for  muscles  of  the,  612 

Ballet-dancer's  cramp,  565 

Barany's  test  for  vertigo,  175 

Basal  ganglia,  tumors  of  the,  460 

Basedow's  disease,  553 

Baths    in     the    treatment     of    nervous 

diseases,  62 
Batteries,  electric,  65 
Beard's  disease,  514 
Bell's  palsy,  110 
Bends,  the,  220 
Beriberi,  85 
Birth  palsies,  451 
Blepharospasm,  109 
Blindness,  mind,  368 

sign,  368 

word,  368 
Blood-supply  of  the  brain,  353,  356 

of  the  peripheral  nerves,  11 

of  the  spinal  cord,  210 
Brachial  nerves,  diseases  of,  132 
paralysis  of,  133 

neuralgia,  182 

plexus,  anatom3^  of  the,  131 


INDEX 


615 


Brachial  plexus,  sensory  neuroses  of  the, 

182 
Brain,  abscess  of  the,  395 

actinomycosis  of  the,  467 
afferent  tracts,  350,  351 
ansemia  of  the,  393 
anatomy  of  the,  333 
aneurisms  of  the,  473 
angioma  of,  470 
association  centres,  362 

fibres  of,  341 
associative  function  of  the,  363 
bilateral  representation,  359 
blood-supply  of  the,  353,  356 
cancer  of  the,  471 
cells  of  the  cortex,  338 
central  convolution,  358 

ganglia  of,  343 
centres  in  the,  361 
centrum  ovale,  363 
cerebellum,  343,  364 
compression  symptoms,  367 
connecting  tracts  of  the,  347 
convolutions  of  the,  337 
corpora  quadrigemina,  364 

striata,  363 
corpus  callosum,  363 
cortex  of  the,  337 
cranio-cerebral  topography,  600 
cystic  tumors  of  the,  467 
development  of  the,  2,  333 
diagram  of  the  divisions  of  the,  2,  3 
diseases  of  the,  367 
efferent  tracts,  347,  349 
embolism  of  the  arteries  of  the,  438 
enchondroma  of,  470 
endothelioma  of  the,  470 
fibres  of  the  cortex,  337 
fibroma  of  the,  470 
fissures  of  the,  337 
focal  symptoms,  367 
functions  of  the,  358 
glands  of,  345 
glioma  of  the,  468 
gumma  of  the,  467 
hemorrhage  in  the,  424 
hypereemia  of  the,  392 
inflammation  of  the,  395 
irritation  symptoms,  367 
latent  regions  of  the,  365 
lipoma  of,  470 
localization  in  the,  358 


Brain,  malformations  of  the,  374 

meninges  of  the,  352 
diseases  of  the,  367 

motor  tracts  in  the,  347,  348 

occipital  lobe,  361 

optic  thalami,  363 

osteoma  of  the,  470 

parasitic  growths  in  the,  471 

parietal  lobe,  360 

prefrontal  lobes,  358 

projection  fibres,  347 

red  nucleus,  364 

sarcoma  of  the,  470 

sensori-motor  area,  358 

sensory  tracts  in  the,  350,  351 

size  of,  365 

softening  of  the,  acute,  438 
chronic  progressive,  445 

symptoms  of  disease  of  the,  367 

syphilis  of  the,  253,  254 

syphiloma  of  the,  467 

temporal  lobe,  361 

thalamus  opticus,  363 

thrombosis  of  the  arteries  of  the,  438 

topography  of  the,  600 

tubercle  of  the,  467 

tumors  of  the,  454 
cystic,  467 

general  symptoms  of,  456 
local  symptoms  of,  458 
multiple,  466 
of  the  basal  ganglia  and  capsule, 

460 
of  the  cerebellum,  463 
of  the  corpus  callosum,  460 
of  the  corpus  striatum,  460 
of  the  medulla,   463 
of  the  mid-brain,  462 
of  the  occipital  lobes,  459 
of  the  optic  chiasm,  462 
of  the  optic  thalamus,  461 
of  the  optico-striate  region,  460 
of  the  parietal  lobe,  459 
of  the  pineal  gland,  462 
of  the  pituitary  body,  462 
of  the  pons,  463 

of  the  ponto-cerebellar  angle,  466 
of  the  precentral  convolutions,  459 
of  the  prefrontal  area,  459 
of  the  temporal  lobes,  460 

veins  of  the,  356 

weight  of  the,  365 


616 


INDEX 


Brain,  wet,  390 
Brauch-Romberg  symptom,  56 
Brown-Sequard  paralysis,  321 
Brudzinski's  sign,  380 
Bulbar  paralysis,  asthenic,  302 

cerebral,  441 

progressive,  299 

upper,  100 
Bulbospinal  paralysis,  asthenic,  302 

Cachectic  states,  combined  scleroses  of, 

282 
Caisson  disease,  219 
Cancer  of  the  brain,  471 
Capsule,  tumors  of  the,  460 
Caput  obstipum,  119 
Catalepsy,  596 

hysterical,  503 
Cauda  equina,  anatomy  and  diseases  of, 
330 

lesions  at  different  levels,  332 
Causes  of  nervous  diseases,  23 
Cells,  cerebral  cortical,  338 

glia,  12 

nerve,  4 

neuroglia,  10,  11 
Centres,  cerebral,  361 

spinal,  209 
Centrum  ovale,  363 
Cephalalgia,  163 

location   of   pain   according    to    the 
cause,  165 
Cerebellar  ataxia,  56 

hereditary,  291 
Cerebellum,  anatomy  of  the,  343 

functions  of  the,  364 

hemorrhage  in  the,  432 

tumors  of  the,  463 
Cerebral  anaemia,  393 

bulbar  paralysis,  441 

hyperaemia,  392 

palsies  of  children,  447 
Cerebrospinal  fluid,  352 
examination  of,  57 

meningitis,  376 

nerves,  sensory  neuroses  of  the,  145 
Cervical  muscles,  atrophy  of,  129 

nerves,  motor  neuroses  of  the,  126, 
130 
sensory  neuroses  of  the,  180,  182 
Cervico-occipital  pains,  ISO 
Chaddock  reflex,  45 


Charcot     Marie     type     of     progressive 
hereditary    muscular    atrophy, 
298 
Charcot's  disease,  304 
Chemistry  of  the  nervous  system,  21 
Chocked  disc,  156 
Chokes,  the,  220 
Chorea,  535 

dancing,  540 

electric,  540 

hereditary,  540 

Huntington's,  540 

insaniens,  538 

major,  540 

maniacal,  538 

of  the  larynx,  541 

paralytic,  538 

procursive,  540 

senile,  538 

Sydenham's,  535,  and  see  Sydenham' s 
chorea. 
Choreic  movements,  33,  45 
Chromatin  network,  7 
Chromophilic  granules  of  the  nerve  cell,  6 
Cigarmakers'  cramp,  564 
Circumflex  nerve,  paralysis  of  the,  138 
Civilization  as  a  factor  in  the  etiology  of 

nervous  diseases,  25 
Clarionet  players'  cramp,  564 
Claustrophobia,  508 

Climate  as  a  factor  in  the  etiology  of 
nervous  diseases,  25 

in  the  treatment  of  nervous  diseases, 
64 
Clonus,  ankle,  49 
Coccygodynia,  197 
Collaterals,  10 

Columns  of  the  spinal  cord,  200,  203 
Coma,  apoplectic,  425 
Compression  paralysis,  138 
Compulsion,  510 
Compulsive  insanity,  508 

mania,  510 
Condition,  as  a  factor  in  the  etiology  of 

nervous  diseases,  24 
Conjugate  deviation  of  the  eyes,  defini- 
tion of,  99 

spasmodic,  104 
Constitutional  inferiority,  490 
Contracture,  definition  of,  33 

hysterical,  500 
Convergence,  paralysis  of,  101 


INDEX 


617 


Convulsions,  32 

clonic,  32 

epileptic,  476,  504 

hysterical,  494 

tonic,  32 
Convulsive  tic,  33 
Coprolalia,  541 

Cord,  spinal.    See  Spinal  cord. 
Corpora  quadrigemina,  364 
Corpus  callosum,  363 

tumors  of  the,  460 

striatum,  363 

tumors  of  the,  460 
Cortex,  cerebellar,  344 

cerebral,  337 
Cramps,  32 

occupation,  564 

writers',  560 
Crampton  test,  519 
Cranial  nerves,  disorders  of  the,  95 
Cranio-cerebral  topography,  600 
Cranium,  table  of  measurements  of  the, 

43 
Cretinism,  583 

Crises  in  locomotor  ataxia,  265 
Current,  electrical,  employed  in  the  treat- 
ment of  nervous  diseases,  65 

sinusoidal,  66 

strength,  definition  of,  65 
Cutaneous  sensation,  to  test,  51 

sensory  nerves,  distribution  of,  53, 
54 
tracts,  350 
Cyclopia,  375 
Cyclopegia,  101 
Cystic  tumors  of  the  brain,  467 
Cytoplasm,  6 

Dead  fingers,  197 

in  writers'  cramp,  562 
Deafness,  nervous,  172 

word,  368 
Debiles,  24 
Degeneracy,  41 
Degenerates,  24 

Degeneration,  as  a  factor  in  tlie  etiology 
of  nervous  diseases,  23 

of  nerves,  76 

of  nervous  tissue,  28 

of  optic  nerve,  156 

reactions  of,  68 

stigmata  of,  41 


Degeneration,  Wallerian,  76 
Degenerative  nervous  diseases,  474 
De  Lepinaj^'s  sign,  381 
Dementia  paralytica,  403 
Dendrites,  5,  13,  16 

cellupetal  impulses  in  the,  16 
Deviation,  24 

conjugate,  99 
Diagnosis,  electro-,  67 

in  nervous  diseases,  39 
Diaphragm,  paralysis  of  the,  130 
Diathesis,  as  a  factor  in  the  etiology  of 
nervous  diseases,  25 

contractural,  500 

psychopathic,  490 
Diencephalon,  2,  3,  334,  335,  336 
Diet,  for  the  nueropathic,  61 
Digiti  mortui,  197 

in  writers'  cramp,  562 
Diplegia,  451 

definition  of,  34 

hereditary  cerebral,  316 

infantile,  447 
Diplopia,  definition  of,  99 
Diseases  of  the  brain,  367 
Divers'  paralysis,  219 
Dizziness,  174 
Dorsal  nerves,  anatomy  of  the,  141 

motor  neuroses  of  the,  141 
Double  vision,  99 
Doubting  mania,  508 
Dreams,  590 
Drivers'  spasm,  564 
Dropfoot,  144 
Drowsiness,  morbid,  595 
Drunkenness,  sleep,  591 
Du  Bois,  method  of,  72 
Duchenne  Aran's  disease,  293 

muscular  atrophy  of,  308 
Dura  mater,  cerebral,  352 
Dural  hemorrhages,  429 
Dynamometer,  42 
Dyssesthesia,  definition  of,  37 
Dysphagia,  115 

Dystonia  musculorum  deformans,  545 
Dystrophies,  hereditary,  308 

juvenile,  of  Erb,  308,  314 

progressive  muscular,  292,  307 

Ear,  noises  in,  173 
Echokinesis,  541 
Echolalia,  541 


618 


INDEX 


Eclampsia,  474 

Educational  muscular  movements,  for  the 

neurasthenic,  63 
Electricity,    appliances    for    the    thera- 
peutic use  of,  65 

in  the  treatment  of  nervous  diseases, 
65,  69,  70 

methods  of  application  of,  67 

terms  employed  in  relation  to,  65 
Electrodes,  67 
Electro-diagnosis,  67 
Electromotive  force,  definition  of,  65 
Electrotherapeutics,  70 
Electrotonus,  21 
Embohsm,  cerebral,  438 
Encephalitis,  acute  non-suppurative,  401 

acute  suppurative,  395 

hemorrhagic,  401 
Encephalocele,  375 
Encephalon,  336 
End-brush,  6,  10 

-buds,  6 

-organs,  20 
Endothelioma  of  the  brain,  470 
Enteritis,  mucous,  521 
Enteroptosis,  521 
Epicritic  fibres,  19 

sensation,  19 

sensibility,  19 

tests  for,  55 
Epilepsia  tar  diva,  481 
Epilepsy,  474 

abortive  attack,  478 

acute,  474 

association  diseases,  480 

aura,  478 

convulsion,  476,  504 

course,  483 

diagnosis,  482 

etiology,  474 

grand  mal,  474,  481 

haut  mal,  481 

hystero-,  474,  502 

idiopathic,  474 

Jacksonian,  474,  478 

laryngeal,  178 

matutinal,  479 

mental  condition  in,  479 

minor  attack,  477 

onset,  476 

partial,  474,  478 

pathology,  482 


Epilepsy,  petit  mal,  474,  476,  477,  481 

physical  condition  in,  480 

procursive,  477 

prognosis,  483 

psychical,  474,  481 

symptomatic,  474 

symptoms,  476 

treatment,  483 

types,  481 
Epileptiform  neuralgia,  161 
Epiphysis  cerebri,  346 
Erb's  juvenile  drystrophy,  308,  314 

palsy,  134 

syphilitic  spinal  paralysis,  231 
Erroneous  projection,  definition  of,  98 
Erythromelalgia,  195 
Esophoria,  definition  of,  103 
Etiology  of  nervous  diseases,  23 
Examination,    methods    of,    in    nervous 

diseases,  39 
Exercise,  for  the  neurasthenic,  62 
Exophoria,  definition  of,  103 
Exophthalmic  goitre,  553 
Exsomnia,  587 
Eye,  motor  nerves  of  the,  95 
disorders  of,  97,  100 

muscular  asthenopia  and  insufficien- 
cies of  the,  103 

spasmodic  diseases  of  the  muscles  of 
the,  104 

Face,  unilateral  hypertrophy  of,  315 
Facial  hemiatrophy,  progressive,  576 

hemihypertrophy,  progressive,  577 

herpes,  163 

nerve,  anatomy  of  the,  106 
diseases  of  the,  107 

palsies,  110 

spasm,  107,  110 
Facio-scapulo-humeral  muscular  atrophy, 

314 
Fajani's  disease,  553 
Fallopian  neuritis,  112 
Family  nervous  diseases,  315 
Faradic  current,  68 
Festination,  570 
Fever,  hysterical,  502 
Fibres,  nerve,  8 
Fibrillary  tremor,  22 
Fibroma  of  the  brain,  470 
Fibro-neuromata,  multiple,  91 
Finger  pains,  186 


INDEX 


619 


Fingers,  dead,  197 

in  writers'  cramp,  562 
Fixed  ideas,  509. 
Flushing,  163 
Flute  players'  cramp,  564 
Foerster's  shifting  type,  519 
Forced  movements,  34 
Forearm,  cord  centres  for  muscles  of  the, 

610 
Forearm  pains,  186 
Forebrain,  336 

Foot,  cord  centre  for  muscles  of  the,  612 
Fothergill's  neuralgia,  161 
Fourth  nerve,  anatomj'-  of  the,  95 

paralysis  of  the,  102 
Foville's  parah'sis,  443 
Fractures,     spontaneous,     in    locomotor 

ataxia,  266 
Freud's  method,  71 
Friedreich's  ataxia,  286 

myoclonus  multiplex,  542 
Frohlich  syndrome,  578 
Functional  nervous  diseases,  474 

Galvanic  batteries,  67 

current,  68 
Gangrene,  symmetrical,  197 
General  paralysis  of  the  insane,  403,  and 
see  General  paresis. 
paresis,  403 

acute  tj^pe,  406 
dementing  type,  408 
depressed  type,  408 
diagnosis,  410 
etiology,  403 

meningo-vascular  type,  408 
pathology",  410 
prognosis,  412 
serology  of,  414 
sj-mptoms,  404,  406 
treatment,  414 
Gerlier's  disease,  178 
Giddiness,  174 
Glioma  of  the  brain,  468 
Gliosis,  29,  325 
Globus  hystericus,  493 
Glosso-labio-laryngeal  paralysis,  299 
Glossopharyngeal  nerve,  anatomy  of  the, 
115 
motor  neuroses  of  the,  115 
sensorv'  neuroses  of  the,  179 
Glossoplegia,  124 


Gnosia,  37 

Goitre,  exophthalmic,  553 
Gordon  reflex,  45 
Graves'  disease,  553 
Gumma  of  the  brain,  467 

Habit  as  a  factor  in  the  etiology  of  ner- 
vous diseases,  25 
Hgematomyelia,  218 
Hsematorrhachis,  217 
Hsemidrosis,  definition  of,  38 
Hand,    cord   centres  for  muscles  of  the, 

610 
Head,  cord  centres  for  muscles  of  the,  607 

noises  in,  173 
Head's  zones,  191 
Headache,  163 

location  of  pain  in,  according  to  the 
cause,  165 

morning,  166 

sick,  167 
Hearing,  centres  for,  362 

hysterical  disturbances  of,  497 
Heart  arm  pains,  186 
Heine-Medin  disease,  85,  245 

type  of  encephalitis,  401 
Hemiageusia,  179 
Hemianopsia,  157 
Hemiatrophy,  facial,  576 

progressive  lingual,  125 
Hemicrania,  167 
Hemihj^pertrophy,  315 

progressive  facial,  577 
Hemiopic  pupillary  reaction,  158 
Hemiparaplegia,  321 
Hemiplegia,  424,  427 

definition  of,  34 

hephaestic,  564 

hysterical,  498 

infantile,  447 

intermittent,  439 

peduncular,  442 

senile,  446 

sine  materia,  439 
Hemorrhage,  cerebral,  424 

spinal,  217,  218 
Hephasstic  hemiplegia,  564 
Hereditary  cerebellar  ataxia,  291 

chorea,  540 

nervous  diseases,  315 

spastic  paraplegia,  291 

spinal  ataxia,  286 


620 


INDEX 


Heredity  in     the     etiology'     of     nervous 

diseases,  23 
Herpes,  facial,  163 

zoster,  188 
Heterophoria,  definition  of,  103 
Heteropia,  216 

spinal,  216 
Hiccough,  129 
Hind  brain,  336 
Hoffman  reflex,  49 
Hoover's  sign  of  hemiplegia,  435 
Horner  syndrome,  102 
Hughling-Jackson's  syndrome,  445 
Hunt  syndrome,  171 
Huntington's  chorea,  540 
Hutchinson  pupil,  430 
Hydrencephalocele,  375 
Hydrocephalus,  387 

acquired,  389 

chronic,  primary,  388 

external,  387 

internal,  387 

secondary,  389 
Hydromyelia,  324 
Hydrophobia,  551 
Hydrorrhachis  externa,  215 

interna,  215 
Hydrotherapy  in  nervous  diseases,  62 
Hygiene  of  the  nervous  system,  60 
Hypersemia,  cerebral,  392 

meningeal,  375 

of  nerves,  75 
Hypersesthesia,  definition  of,  37 

hysterical,  497 

ocular,  157 

retinal,  157 
Hyperalgesia,  definition  of,  37 
Hyperidrosis,  definition  of,  38 
Hyperosmia,  152 
Hyperphoria,  definition  of,  103 
Hyperthyroidism,  553 
Hypertrophy,  pseudo-muscular,  310 

unilateral  of  face,  315 
Hypnotism,  71,  593 

lethargic,  594 

major,  593 

minor,  593 
Hypochondriasis,  511 
Hypoglossus  nerve,  anatomy  of  the,  123 

motor  neuroses  of  the,  123 
Hypophysis  cerebri,  345 
Hypotonia,  56,  545 


Hysteria,  491 

anaesthesia,  495 
aphonia,  499 
blue  oedema,  502 
catalepsy,  503 
contractures,  500 
convulsions,  494,  504 
crises,  494 
diagnosis,  503 
etiology,  491 
fever  in,  502 
globus,  493 
hearing  in,  497 
hypersesthesia,  497 
major,  491,  494 
mental  state  in,  503 
minor,  491 

motor  symptoms,  498 
myasthenia,  500 
neuralgia,  497 
paralyses,  498 
pathology,  503 
prognosis,  504 
psj^chasthenia,  503,  511 
sensory  symptoms,  495 
symptoms,  491 

of  the  crises,  494 

of  the  interparoxysmal  state,  495 
taste  disturbance  in,  497 
topalgia  in,  498 
trance,  503 
traumatic,  533 
treatment,  504 
tremor  in,  501 
trophic  disorders,  502 
vasomotor  symptoms,  502 
visceral  symptoms,  502 
visual  disturbances  in,  496 
Hystero-epilepsy,  474,  502 

Ignipedites,  85 
Impulsive  insanity,  508 

manias,  510 

psychoneurosis,  510 
Infantile  hereditary  bulbar  palsy,  302 

paralysis,  236 
Infection  as  a  factor  in  the  etiology  of 

nervous  diseases,  26 
Inferiority,  constitutional,  490 
Inflammation,  of  brain,  395 

of  spinal  cord,  224 

of  nerves,  76 


INDEX 


621 


Insane,    general    paralysis    of,    403,  and 

see  General  paresis. 
Insomnia,  587 

Insufficiencies,  muscular,  of  the  eye,  103 
Intention  tremor,  32 
Intercostal  nerves,   sensory  neuroses   of 

the,  187 
Interfascicular  arcades,  12 
Iridoplegia,  101 
Irritability  of  a  nerve,  21 
Irritation,  spinal,  518,  523 

Jaw -jerk,  48 

Kakke,  85 
Kernig's  sign,  380 
Klumpke's  paralysis,  125 
Knee-jerk,  47 
Korsakoff's  psychosis,  83,  84 

Lacrymation,  163 
Lacunar  degeneration,  446 
Landouzy-Dejerine  muscular  dystrophy, 

308 
Landry's  paralysis,  245 
Laryngeal  epilepsy,  syncope,  or  vertigo, 

178 
Larynx,  chorea  of  the,  541 
Latent  regions  of  the  brain,  365 
Lateral  sclerosis,  279 

amyotrophic,  304  . 
Lead  palsy,  138,  146 

Leg,  cord  centres  for  muscles  of  the,  612 
Leptomeningitis,  cerebral,  376 

spinal,  223 
Lethargy,  586 
Levator  palpebrse,  paralysis  of  the,  102 

spasm  of  the,  105 
Leyden-Moebius  muscular  dystrophy, 

308,  309,  312 
Lingual  hemiatrophy,  progressive,  125 

paralysis,  124 

spasms,  124 
Little's  disease,  280 
Localization,  cerebral,  358 
Lockjaw,  106 
Locomotor  ataxia,  257 

ankle  tendon,  reflex  in,  261 

arthropathies  of,  266 

ataxic  stage,  258 

cerebral  symptoms  in,  269 

complications,  270 


Locomotor  ataxia,  course  of,  270 

crises  in,  265 

definition,  257 

diagnosis,  275 

etiology,  257 

eye  symptoms,  of  263 

forms,  257 

fractures  in,  266 

gait  in,  261 

hemiplegia  in,  269 

hydrotherapy  in,  277 

hypotonia  in,  261,  262 

initial  stage,  258 

joint  affections  in,  266 

laryngeal  crises  in,  265 

muscular  atrophies  in,  269 

nwoclonic  spasms  in,  261 

myokimia  in,  261 

neuralgia  in,  262 

optic  atrophy  in,  263 

pains  in,  262 

paralytic  stage  of,  259 

paresis  in,  270 

patellar  tendon  reflex  in,  261 

pathological  anatomy,  270 

pathology,  272 

pre-ataxic  stage,  258 

prognosis,  275 

sexual  power  in,  269 

symptoms,  258,  260 

syphilis  in  the  etiology  of,  257,  272 

treatment,  276 

trophic  disturbances  in,  268 
Lower  extremities,  cord  centres  for  the 

muscles  of,  612 
Lumbar  nerves,  anatomy  of  the,  141 

motor  neuroses  of  the,  143 

sensory  neuroses  of  the,  189 
Luetic  melancholia,  253 

neurasthenia,  253 

type  of  spinal  atrophy,  297 
Lumbo-abdominal  neuralgia,  189 

Macewen's  sign,  382 
Mammary  neuralgia,  188 
Mania,  compulsive,  510 

doubting,  508 

impulsive,  510 
Massage   in   the   treatment    of   nervous 

diseases,  63 
Mastodynia,  188 
Masturbation,  530 
Median  nerve,  paralysis  of  the,  140 


622 


INDEX 


Medulla  oblongata,  functions  of  the,  365 

thrombosis  and  softening  of  the,  444 

tumors  of  the,  463 
Melancholia,  luetic,  253 
Meniere's  disease,  176 
Meninges,  cerebral,  352 

anaemia  of  the,  375 
blood-supply  of  the,  353 
diseases  of  the,  367,  375 
functions  of  the,  352 
hypersemia  of  the,  375 
malformations  of,  374 

spinal,  inflammation  of  the,  221 
Meningitis,  alcoholic,  390 

cerebrospinal,  376 
epidemic,  378 

epidemic  cerebrospinal,  378 

external  spinal,  222 

lepto-,  376 

pachy-,  222 

serous,  390 

spinal,  221 

tuberculous,  386 
Meningocele,  cerebral,  375 

spinal,  215 
Meningo-myelitis,  232 

-myelocele,  215 

-vascular  lues,  serology  of,  413 
Meralgia,.  190 
Mesencephalon,  2,  3,  336 
Mesmerism,  593 
Metencephalon,  3,  336 
Micrencephaly,  375 
Microcephaly,  375 
Micromyelia,  217 
Mid-brain,  336 

softening  of,  442 
Migraine,  167 

fulgurating,  168 
Migrating  neuritis,  141 
Millard-Gubler  syndrome,  444 
Milkers'  spasm,  564 
Milliampere,  definition  of,  65 
Milliamperemeter,  65 
Mimic  tic,  107 
Moebius'  symptom,  556 
Mogophonia,  564 
Mononeuritis,  80 
Monoplegia,  definition  of,  34 
Morbid  compulsion,  510 

fear,  508 

impulses,  510 


Morton's  neuralgia,  196 

Morvan's  disease,  141 

Motility,  disordered,  examination  for,  42 

Motor  disorders  of  cranial  nerves,  95 

tracts  in  the  brain,  347,  348 
Movements,  associated,  34 
choreic,  33 

educational,  for  neurasthenics,  63 
forced,  34 
Mucous  enteritis,  521 
Multiple  neuritis,  80  and  see  Polyneuritis. 
sclerosis,  417 

aborted  types  of,  421 
Muscles,     tables    showing     innervation, 

functions,  etc.,  of  the,  607 
Muscular  asthenopia  and  insufficiencies, 
103 
atrophy,  arthritic,  316 

facio-scapulo-humeral,  361 
hereditary     progressive     of     the 

peroneal  type,  298 
occupation,  317 
progressive,  292,  293 
spastic  form  of,  304 
dystrophies,  progressive,  292 
Landouzy-Dejerine  type  of,  308 
Leyden-Moebius  type  of,  308,  309, 
312 
Musculo-spiral  nerve,  paralysis  of  the,  138 
Musicians'  cramp,  564 
Myasthenia  gravis,  302 
Myatonia,  545 
Myelencephalon,  3,  336 
Myelin  sheath,  8 
Myelitis,  224 
acute,  225 

definition,  225 
diagnosis,  230 
etiology,  225 
forms,  225 
pathology,  228 
prognosis,  230 
symptoms,  226 
transverse,  231 
treatment,  231 
central,  symptoms,  231,  233 
chronic,  231 
diagnosis,  234 
etiology,  231 
forms,  231 
pathology,  233 
prognosis,  235 


INDEX 


623 


Myelitis,  chronic,  symptoms,  232 
sypiiilis  in  etiology  of,  231 
syphilitic  spinal  paralysis,  232 
treatment,  235 

compression,  231 
symptoms,  233 

diffuse,  231 

disseminated,  231 

marginal,  231 

periependymal,  symptoms,  233 

syphilitic,  231 

transverse,  231 
Myelomalacia,  224 
Myoclonia,  32,  535 

fibrillary,  542 
Myoclonus,  535 

multiplex,  of  Friedreich,  542 
Myoidema,  definition  and  significance  of, 

34 
Myokymia,  32 

disorders,  535 
Myopathic  face,  314 
Myotonia,  535,  543 

acquisita,  543 

congenita,  315,  544 

symptomatica,  543,  545 
Myotonus,  535 
Mysophobia,  508 
Myxoedema,  581 

Narcolepsy,  596 

Neck,  anatomy  of  muscles  and  nerves  of 
the,  127 
cord  centres  for  muscles  of  the,  607 
Neck  pains,  180 
Necrosis,  28 
Negri  bodies,  551 

Nerve  or  nerves,  abducens,  anatomy  of 
the,  95 
paralysis  of  the,  102 
acoustic,  anatomy  of  the,  171 

neuroses  of  the,  171 
afferent,  18 
anaemia  of,  75 
angina  of,  75 
auditory,  anatomy  of  the,  171 

neuroses  of  the,  171 
brachial  plexus,  anatomy  of  the,  131 
paralysis  of  the,  133 
sensory  neuroses  of  the,  182 
centrifugal,  18 
centripetal,  18 


Nerve  or  nerves,  cerebrospinal,    sensory 
neuroses  of  the,  145 
cervical,  anatomy  of  the,  119,  126, 
127,  130 

motor  neuroses  of  the,  126 

sensory  neuroses  of  the,  180,  182 
circumflex,  paralysis  of  the,  138 
cranial,  disorders  of  the,  95 
cutaneous  sensory,   distribution  of, 

53,  54 
degeneration  of,  76 

neuritic,  78 

of  Nissl,  78 

primary,  76 

secondary,  76 

toxic,  78 

Wallerian,  76 
doi'sal,  anatomy  of  the,  141 

motor  neuroses  of  the,  141 
efferent,  18,  20 
eighth,  anatomy  of  the,  171 

neuroses  of  the,  171 
eleventh,  anatomy  of  the,  116 

diseases  of  the,  117,  119,  122 
excito-reflex,  19 
extero-ceptive,  17,  19 
facial,  anatomy  of  the,  106 

diseases  of  the,  171 
fifth,  anatomy  of  the,  159 

motor  neuroses  of  the,  106 

sensory  neuroses  of  the,  160 
fourth,  anatomy  of  the,  95 

paralysis  of  the,  102 
glossopharyngeal,    anatomy    of   the, 
115 

motor  neuroses  of  the,  115 

sensory  neuroses  of  the,  179 
hypersemia  of,  75 
hyperplasia  of,  90 
hypertrophy  of,  90 
hypoglossus,  anatomy  of  the,  123 

motor  neuroses  of  the,  123 
inflammation  of,  76  and  see  Neuritis. 
ingoing,  18 
inhibitory,  18,  20 
intercostal,  sensory  neuroses  of  the, 

187 
lumbar,  anatomy  of  the,  141 

motor  neuroses  of  the,  143 

sensory  neuroses  of  the,  189 
median,  paralysis  of  the,  140 
motor,  18,  20 


624 


INDEX 


Nerve  or  nerves,  musculo-spiral,  paraly- 
sis of  the,  138 
ninth,  anatomy  of  the,  115 

motor  neuroses  of  the,  115 

sensory  neuroses  of  the,  179 
oculo-motor,  anatomy  of  the,  95 

paralysis  of  the,  98,  100 
olfactory,  anatomy  of  the,  150 

neuroses  of  the,  151 
optic,  anatomy  of  the,  152 

diseases  of  the,  154 
outgoing,  18 
peripheral,  blood-vessels  of  the,  11 

diseases  of  the,  75 
phrenic,  anatomy  of  the,  129 

paralysis  of  the,  130 
pneumogastric,  anatomy  of  the,  116 

diseases  of  the,  117 
posterior  thoracic,  paralj'sis  of  the, 

137 
proprio-ceptive,  17,  19 
regeneration  of,  79 
sacral,  anatomy  of  the,  143 

motor  neuroses  of  the,  144 
sciatic,  neuralgia  of  the,  191 
secretory,  20 
sensory,  19 
seventh,  anatomy  of  the,  106 

diseases  of  the,  171 
sixth,  anatomy  of  the,  95 

paralysis  of  the,  102 
special  sense,  neuroses  of  the,  150 
spinal  accessory,  anatomy  of  the,  116 

diseases  of  the,  117,  119,  122 
spinal,  anatomy  of  the,  126 

motor  neurones  of  the,  126 
suprascapular,  paralysis  of  the,  138 
syphilis  of,  256 
tenth,  anatomy  of  the,  116 

diseases  of  the,  117 
third,  anatomy  of  the,  95 

paralysis  of  the,  98,  100 
thoracic,  anatomy  of  the,  141 

motor  neuroses  of  the,  141 
trigemmus,  anatomy  of  the,  159 

motor  neuroses  of  the,  106 

sensory  neuroses  of  the,  160 
trochlear,  anatomy  of  the,  95 

paralysis  of  the,  102 
tumors  of,  90 
twelfth,  anatomy  of  the,  123 

motor  neuroses  of  the,  123 


Nerve  or  nerves,  ulnar,  paralysis  of  the, 
140 
vagus,  anatomy  of  the,  116 

diseases  of  the,  117 
vestibular,  neuroses  of,  174 
Nerve-cells,  4 
bipolar,  8 
body  of  the,  6 
classification  of,  7 
connection  of,  with  nerve  fibres,  10 
ganglionic,  6 
multipolar,  7 
Nissi  granules,  6 
nucleus  of  the,  6,  7 
physiology  of  the,  18 
processes  of  the,  4 
Nerve-fibres,  8 
central,  9 

connection  of,  with  nerve-cells,  10 
epicritic,  19 
meduUated,  8 
non-medullated,  9 
protopathic,  19 
rate  of  conduction  in,  21 
size  of,  9 
Nervous  deafness,  172 

diseases,  causes  of,  23 

degenerative,  474 

diagnosis  of,  39 

family,  315 

functional,  474 

hereditary,  315 

methods  of  examination  in,  39 

prophylaxis  of,  60 

symptoms  of,  30 

treatment  of,  60 
exhaustion,  514 
system,  anatomy  of  the,  1 

arrangement  of,  2 

autonomic,  3,  13,  14,  15 

blood-vessels  of  the,  11 

central,  13 

chemistry  of  the,  21 

development  of,  333 

histology  of  the,  4 

hygiene  of  the,  60 

neuronic  architecture  of  the,  12 

parasympathetic,  15 

pathology  of  the,  28 

peripheral  divisions  of  the,  3 

physiology  of  the,  18 

sympathetic,  13,  15,  16 


INDEX 


625 


Nervous  system,  sympathetic,  ganglia  of 
the,  3 
syphihs  of  the,  251 
Neuralgia,  147 

brachial,  182 

cervico-occipital,  180 

congestive,  of  the  feet,  195 

epileptiform,  161 

Fothergill's,  161 

hallucinatory,  149 

hysterical,  497 

intercostal,  187 

lumbo-abdominal,  189 

mammary,  188 

Morton's,  196 

plantar,  195 

red,  of  the  feet,  195 

reminiscent,  149 

sciatic,  191 

trigeminal,  160 
Neurasthenia,  514 

angiopathic,  524 

course,  526 

diagnosis,  525 

etiology,  515 

gravis,  525 

local,  524 

luetic,  253 

pathogeny,  525 

pathology,  525 

prognosis,  526 

spinal  irritation,  523 

symptoms,  517 

traumatic,  522,  533 

treatment,  527 
Neuraxon,  5,  13 

cellufugal  impulses  in  the,  13,  16 
Neurilemma,  8 

ascending,  76 

brachial,  182 

degenerative,  76 

descending,  76 

diffuse,  76 

disseminated,  76 

Fallopian,  112 

interstitial,  76,  77 

migrating,  76,  141 

multiple,  80,  and  see  Polyneuritis. 

peri-,  76 

retrobulbar,  155 

sciatic,  191 
segmental,  76 


Neurofibromata,  91,  93 
Neurofibromatosis,  91 
Neuroglia,  10,  11 
Neuromata,  91 

amputation,  93 
etiology,  93 
false,  93 
fibro-,  95 
multiple,  91 
plexiform,^93 
symptoms,  93 
treatment,  94 
true,  91 
Neurons,  1,  5,  6,  12 
associative,  16,  20 
central,  20 
collaterals  of  the,  5 
diagram  showing  the  arrangement  of 

the,  17 
end-brush,  6,  10 

-buds,  6 
intercentral,  20 
peripheral,  18 
terminal  aborization,  6 
Neuropathic  condition  or  diathesis,  23 

constituent,  41 
Neuro-retinitis,  154 
Neuroses,  definition  of,  30 
motor,  30 
occupation,  560 
of  nerves  of  special  sense,  150 
professional,  560 
secretory,  30,  38 
sensorjr,  30 
sexual,  530 
thermic,  30 
trophic,  30,  197 
vaso-motor,  30,  197 
vestibular,  174 
Nictitating  spasm,  110 
Nightmare,  590 
Night  palsy,  146 
terrors,  591 
Nissl  granules,  6 
Nerve  degeneration,  78 
Numbness,  waking,  146 
Nyctalopia,  157 
Nystagmus,  45,  104 


Obsession,  509 

Occipital  lobes,  tumors  of,  459 


626 


INDEX 


Occupation  as  a  factor  in  the  etiology  of 
nervous  diseases,  24 

fears,  509 

muscular  atrophies,  317 

neuroses,  560 
Ocular  hypersesthesia,  157 

muscles,  spasmodic  diseases  of,  104 
Oculo-cardiac  reflex,  49 

-motor  nerve,  anatomy  of  the,  95 
paralysis  of  the,  98,  100 
CEdema,  angioneurotic,  583 

blue,  of  hysteria,  502 

circumscribed,  583 

fugax,  583 
Ohm,  definition  of,  65 
Ohm's  law,  65 
Olfactory  nerve,  anatomy  of  the,  150 

neuroses  of  the,  151 
Olivary  bodies,  functions  of  the,  365 
Onomatomania,  510 
Ophthalmoplegias,  98,  100 

progressive,  102 
Oppenheim  reflex,  45 
Optic  atrophy,  156 

in  locomotor  ataxia,  263 

chiasm,  tumors  of  the,  462 

nerve,  anatomy  of  the,  152 
diseases  of  the,  154 

thalami,  tumors  of  the,  461 
Optic o-striate    region,     tumors    of    the, 

460 
Orthophoria,  definition  of,  103 
Osteoma  of  the  brain,  470 
Osteopathy,    in    treatment    of    nervous 
diseases,  64 

Pachymeningitis  externa,  cerebral,  375 
spinal,  222 

hypertrophic,  222 

interna,  222 
Pain,  sense,  testing  the,  55 
Pains,  cervico-occipital,  180 

finger,  186 

forearm,  186 

heart  arm,  186 

lancinating,  of  locomotor  ataxia,  262 

lumbo-abdominal,  189 

neck,  180 

transferred,  diagram  of  location  of, 
147 
Palate,  cord  centres  for  muscles  of  the. 
607 


Pallor,  163 
Palsy,  arm,  133 
Bell's  ,110 
bulbar,  upper,  100 
Erb's,  134 
facial,  110 
lead,  138,  146 
night,  138,  146 
nuclear,  208 
leg,  144 
peripheral,  208 
radicular,  208 
root,  208 
sacral,  144 
shaking,  567 
Papillitis,  154 
Para-epilepsy,  479 
Parsesthesia,  145 
aero-,  146 
cephalic,  146 
cerebral,  146 
definition  of,  37,  145 
local,  146 
psychic,  146 
trigeminal,  163 
Parageusia,  180 
Paralysis,  abducens,  102 
acoustic,  172  ' 
acute  ascending,  245 
agitans,  567 

course,  572 

diagnosis,  573 

duration,  572 

etiology,  567 

eye  movements  in,  571 

festination  in,  570 

forms  of,  572 

handwriting  in,  571 

muscular  weakness  in,  571 

pathology,  574 

prognosis,  574 

rigidity  in,  571 

symptoms,  569 

treatment,  575 

tremor  in,  570 
alcoholic,  80 

analgesic,  with  whitlow,  141 
arsenical,  80 
asthenic  bulbar,  302 

bulbospinal,  302 
brachial,  133 
Brown-Sequard,  321 


INDEX 


627 


Paralysis,  bulbar,  asthenic,  302 

cerebral,  441 

progressive,  299 

upper,  100 
bulbospinal,  asthenic,  302 
cerebral  bulbar,  441 

of  children,  447 
compression,  138 
definition  of,  34 
diphtheritic,  80 
divers',  219 
Erb's,  134 

syphilitic  spinal,  231 
facial,  110 
Foville's,  443 

glosso-labio-laryngeal,  299 
general,  of  the  insane,  403 
hysterical,  498 
infantile  spinal,  236 
Klumpke's,  125 
Landry's,  245 
lead,  138,  146 
lingual,  124 
oculomotor,  98,  100 
of  convergence,  101 
of  the  anterior  crural  nerve,  143 
of  the  cervical  muscles,  129 
of  the  circumflex  nerve,  138 
of  the  diaphragm,  130 
of  the  iris,  101 

of  the  levator  palpebrse  muscle,   102 
of  the  lumbar  nerves,  143 
of  the  median  nerve,  140 
of  the  musculo-spiral  nerve,  138 
of  the  obturator  nerve,  143 
of  the  phrenic  nerve,  130 
of  the  posterior  thoracic  nerve,  137 
of  the  sacral  nerves,  144 
of  the  spinal  accessory  nerve,  122 
of  the  suprascapular  nerve,  138 
of   the   sympathetic    nerves    of    the 

eye,  102 
of  the  ulnar  nerve,  140 
progressive  bulbar,  299 
spastic,  spinal,  279 
syphilitic  spinal,  232 
testing  for,  42 
types  of,  44 
Paramyotonia,  545 
ataxia,  545 
congenital,  545 
symptomatic,  545 


Paraphasia,  370 
Paraplegia,  definition  of,  34 

flaccid,  245 

senile,  244 

spastic  senilis,  244 

spinal,  279 
Paresis,  definition  of,  34 

general,  403 
Paridrosis,  definition  of,  38 
Parietal  lobe,  tumors  of  the,  459 
Parkinson's  disease,  567 
Parosmia,  152 
Patella  tendon  reflex,  47 
Pathology,  general,  of  the  nervous  sys- 
tem, 28 
Pavor  nocturnus,  591 
Pedo-dynamometer,  42 
Peduncular  hemiplegia,  442 
Perineuritis,  76 
Perineurium,  8 
Peripheral  nerves,  diseases  of  the,  75 

muscular  atrophy  in,  79 

pathology,  75 

symptoms,  79 

vasomotor  and  trophic  neuroses,  197 
Pernicious     anaemia,     combined     spinal 

scleroses  of,  282 
Phaiynx,  cord  centres  for  muscles  of  the, 

607 
Photographers'  cramp,  565 
Phrenic  nerve,  anatomy  of  the,  129 

paralysis  of  the,  130 
Physiology,  general,  of  the  nervous  sys- 
tem, 18 
Pial  hemorrhages,  431 
Pianists'  cramp,  564 
Pineal  gland,  346 

disorders  of,  578 

tumors  of,  462 
Pituitary  body,  345 

diseases  of,  577 

tumors  of,  462 
Plantar  neuralgia,  195 
Plexus,  brachial,  anatomy  of  the,  131 

paralysis  of,  133 

sensory  neuroses  of  the,  182 
Plexuses,    vascular,    of    the  spinal   cord, 

212 
Pneumogastric   nerve,   anatomy   of  the, 
116 

diseases  of  tlic,  117 
Pododynia,  197 


628 


INDEX 


Poison,    as   a  factor  in   tlie   etiology   of 

nervous  diseases,  26 
Policeman's  disease,  196 
Polioencephalitis,  240 

ataxic,  241 

hemorrhagic,  401 

superior,  100 
Poliomyelitis,  acute,  236 

abortive,  241 

ascending,  240 

bulbar,  240 

chronic  anterior,  243,  297 

epidemic,  236 

spinal,  236 
Polyneuritis,  80 

acute  pernicious,  85 

alcoholic,  81 

complicating  forms,  90 

diagnosis,  87 

diphtheritic  neuritis,  83 

endemic  type,  85 

epidemic  type,  85 

etiology,  80 

forms  of,  80 

malarial,  85 

mental  symptoms,  84 

motor  symptoms,  83 

pathology,  86 

prodromata,  82 

prognosis,  89 

pseudo-tabetic  type,  84 

sensory  motor  type  of,  80 

symptoms,  82 

treatment,  89 
Pons  Varolii,  functions  of  the,  365 

thrombosis  and  softening  of  the,  443 

tumors  of  the,  463 
Ponto-cerebellar  angle,  tumors  of  the,  466 
Porencephaly,  375 

Posterior   spinal   sclerosis,    257,   and  see 
Locomotor  ataxia. 

thoracic  nerve,  paralysis  of  the,  137 
Prsedormitial  shocks,  597 
Prefrontal  area,  tumors  of  the,  459 
Pressure  sense,  testing  the,  52 
Professional  neuroses,  560 
Prophylaxis  of  nervous  diseases,  60 
Prosencephalon,  2,  3,  336 
Prosopalgia,  161 
Protagon,  22 
Protopathic  fibres,  19 

sensation,  19 


Protopathic  sensibility,  19 
testing  for,  55 

system,  19 
Pseudo-bulbar  paralysis,  441 
Pseudo-muscular  hypertrophy,  310 
Pseudo-paresis,  408 

alcoholic,  409 
Psychasthenia,  503,  507 

hysteria  and,  503 
Psychic  analysis,  method  of,  71 
Psychoneuroses,  488 
Psychoneurosis,  impulsive,  510 

spinal,  523 

traumatic,  522 
Psychopathic  diathesis,  490 
Psychoses,  30 

sexual,  530 
Psychotherapy,  70 

by  emotional  shock,  73 

empirical,  72 

philosophic,  73 
Ptosis,  102 

morning,  102 

waking,  102 
Pupil,  Argyll  Robertson,  49 

hemiopic  reaction  of  the,  158 
in  locomotor  ataxia,  264 

Hutchinson,  430 
Putnam's  type  of  combined  sclerosis,  282 

Quincke's  disease,  583 

Rabies,  551 

paralytic,  552 
Rachischisis  posterior,  214 
Radiant  energy,  70 
Railway  spine,  533 
Raynaud's  disease,  197 
Reaction,  electrical,  diagnostic   table  of, 
69 

of  degeneration,  67 

time,  21 
Recklinghausen's  disease,  91 
Red  nuclei  of  the  brain,  364 
Re-education,  method  of,  72 
Re-enforcement  of  the  knee-jerk,  48 
Reflex  action,  21,  35 

causes  of  nervous  diseases,  27 
Reflexes,  35 

bone,  48 

deep,  47,  48 

examination  of  the,  45 


INDEX 


629 


Reflexes,  re-enforcement  of,  48 

skin,  45,  46 

superficial,  45,  46 

tendon,  47,  48 
Remak,  fibres  of,  9 
Representation,  bilateral,  359 
Retardation,  mental,  42 
Retrobulbar  neuritis,  155 
Rheostat,  definition  of,  65 
Rhombencephalon,  2,  3 
Rumpf's  symptom,  519 

Sacral  nerves,  anatomy  of  the,  143 

motor  neuroses  of  the,  144 
St.  Vitus's  dance,  535 
Salaam  spasm,  478 
Salivation,  163 
Sarcoma  of  the  brain,  470 
Scapulo-humeral  dystrophy,  314 
Sciatica,  191 

Scleroses,  combined,  of  the  spinal  cord, 
282 

lateral  spinal,  279 
amyotrophic,  304 

multiple,  417 

aborted  types  of,  421 

of  nervous  tissue,  28 

of  spinal  cord,  248 

Putnam's  type  of  combined  spinal, 
282 
Sclerosis,  amyotrophic  lateral,  295 

combined,  of  pernicious  anaemia  and 
cachectic  states,  282 
Senile  hemiplegia,  446 
Sensations,  cutaneous,  methods  of  test- 
ing, 51 

delayed,  37 

disorders  of,  examination  for,  50,  55 

epicritic,  19 

general,  nerves  of,  19 

protopathic,  19 

referred,  37 

reflex,  37 

special,  nerves  of,  19 

transferred,  37 
Senses,  special,  centres  for  the,  361 
Sensori-motor  area  in  the  brain,  358 
Sensory  tracts  in  the  brain,  350,  351 
Sewing  spasm,  564 
Sex  as  a  factor  in  the  etiology  of  nervous 

diseases,  24 
Sexual  neuroses  and  psychoses,  530 


Shaking  palsy,  567 
Shingles,  188 

Shock  as  a  factor  in  the  etiology  of  nerv- 
ous diseases,  25 
Shocks,  prsedormitial,  597 
Shoulder    and    upper    extremity,     cord 

centres  for  muscles  of  the,  608 
Sinusoidal  current,  66 
Skin,  distribution  of  the  sensory  nerves 
of  the,  53,  54 

reflexes,  45,  46 
Skull,  dimensions  and  shape  of  the,  41,  43 

landmarks    of    the,    indicating    the 
imderlying  parts  of  the  brain,  600 
Sleep,  586 

accidents  of,  597 

disorders  of,  586 

disturbances  of,  590 

morbid,  from  organic  disease,  597 

morbidly  deep,  595 

normal,  586 

paroxysmal,  596 

perversions  of,  590 
Sleep  drunkenness,  591 

epilepsy,  596 
Sleeping  sickness,  597 
Smell,  centres  for,  362 

disorders  of,  151 
Smiths'  spasm,  564 
Softening  of  the  brain,  438,  445 

of  the  spinal  cord,  224 
Somnambulism,  592 
Somnambulistic  trance,  594 
Somnolence,  595 
Somnolentia,  591 
Spasm,  facial,  107 

idiopathic  muscular,  34 

lingual,  124 

nictitating,  110 

nodding,  129 

ocular,  104 

of  levator  palpebra;,  105 

oscillating,  129 

salaam,  478 

smiths',  564 

tonic,  535 
facial,  110 
of  neck,  128 

twitching,  535 

winking,  110 
Spasmodic  tics,  541 
Spastic  spinal  paralysis,  279 


630 


INDEX 


Special  associations,  centres  for,  362 

senses,  centres  for,  361 
Spermatorrhoea,  530 
Spina  bifida,  214 

Spinal  accessory  nerve,  anatomy  of  the, 
116 

diseases  of  the,  117,  119,  122 
Spinal  cord,  absence  of,  216 

acute  softening  of  the,  224 

afferent  tracts,  350,  351 

amyotrophic  lateral  sclerosis,  304 

anatomy  of  the,  200 

apoplexy  of,  217 

arteries  of  the,  210,  211,  213 

association  tracts,  204 

asymmetry  of  the,  217 

atrophy,  luetic,  297 

automatic  centres,  209 

blood-supply  of  the,  210 

cavities  in  the,  324 

centres  in  the,  209 

columns  of  the,  200,  203 

composition  of  the,  200 

concussion  of,  500,  533 

degeneration  of  the,  primary,  248 
secondary,  250 
short  tracts  of,  251 

diagnostic  physiology  of,  208 

direct  cerebellar  tract,  206 

diseases  of  the,  214 

double,  217 

efferent  tracts,  204,  347,  349 

fibres,  203 

fissures,  200 

gray  matter  of  the,  201 

hemorrhage  in  the,  217,  218 

heteropia  of,  216 

horns  of  the,  201 

inflammation  of  the  224,  and  see 
Myelitis. 

localization  in  the,  210 

lumbar  puncture  of  the,  58 

malformations  of  the,  214,  216 

meninges  of  the,  200 

inflammation  of  the,  221 

nerve  roots  200,  208 

physiology  of  the,  208 

plexuses  of  the,  212 

pyramidal  tracts,  203,  204 

relations  of  the  different  parts  of  the, 
to  the  peripheral  nerves,  and 
each  other,  208 


Spinal  cord,  root,  ganglia,  200 

sclerosis  of  the,  248 

amyotrophic  lateral,  304 

lateral,  279 

posterior,  257 

Putnam's  tj^pe  of  combined,  282 

softening  of  the,  224 

syphilis  of  the,  251,  254 

topography  of  the,  210 

tracts  of  the,  204 

tumors  of  the,  318,  320 

veins  of  the,  212 

white  matter  of  the,  202 
Spinal  irritation,  518,  523 

nerves,  motor  neuroses  of  the,  126 

puncture,  58 
Spine,  railway,  533 
Spotted  fever,  378 
Stammering,  124 
Status  epilepticus,  477 

vertiginosus,  176 
Stellwag's  symptom,  556 
Stenographers'  cramp,  560 
Stereognosis,  36 

Stereognostic  sense,  testing  of,  55 
Stigmata  of  degeneration,  41,  42 
Strumpell's  reflex,  45 
Stuttering,  124,  129 
Subdural  hemorrhage,  430 
Suprascapular  nerve,  paralysis  of  the,  138 
Sydenham,  chorea  of,  535 

diagnosis,  539 

duration,  538 

etiology,  535 

forms,  538 

pathology,  538 

prognosis,  539 

relapses,  538 

symptoms,  536 

treatment,  539 
Symbolia,  37 
Sympathetic  nervous  sj^stem,  13 

ganglia  of  the,  3 
Symptoms,  general,  of  nervous  disease,  30 

mental,  of  nervous  disease,  31 

motor,  of  nervous  disease,  31 
examination  for,  42 

secretory,  of  nervous  disease,  37,  38 

sensory,  of  nervous  disease,  35 
examination  for,  50 

trophic,  of  nervous  disease,  37 

vasomotor,  of  nervous  disease,  37 


INDEX 


631 


Syncope,  laryngeal,  178 

local,  of  the  extremities,  197 
Syphilis,  hereditary,  256 

laboratory  tests  for,  412 

meningovascular,  253 

of  the  brain,  253,  254 

of  the  nerves,  256 

of  the  nervous  system,  251 

degenerative  processes  following, 
272 

parenchymatous,  256 

prodromal,  253 
Syphilitic  spinal  paralysis,  232 
Syphiloma  of  the  brain,  467 
Syringomyelia,  325 

neuritic  type  of,  141 
Syringomyelocele,  215 

Tabes   dorsaUs,   257,   and   see  Locomotor 

ataxia. 
Tabo-paresis,  270,  408 
Tactile  amnesia,  37 

sense,  testing  the,  51,  55 
Tapir  mouth,  314 
Tarsalgia,  196 
Taste,  centres  for,  362 

disorders  of,  179 

fibres  of  the  facial  nerve,  107 

of    the    glossopharyngeal    nerve, 
115 

hysterical  disturbances  of,  497 
Telegraphers'  cramp,  564 
Telencephalon,  2,  3,  336 
Temperature  sense,  testing  the,  52 
Temporal  lobes,  tumors  of  the,  460 
Tendon  reflexes,  47,  48 
Terminal  aborization,  6 

buttons,  6 
Tetanilla,  547 
Tetanus,  546 
Tetany,  547 

asthenic,  550 

epidemic,  550 

parathyroid,  550 

reflex,  550 

toxic,  550 
Thalamus  opticus,  363 
Therapeutic  talk,  method  of,  72 
Thermo-antesthesia,  definition  of,  36 
Thomsen's  disease,  544 
Thoracic  nerves,  anatomy  of  tlie,  141 

motor  neuroses  of  the,  141 


Thrombosis,  cerebral,  438 

of  medulla,  444 

of  pons,  443 

sinus,  446 
Tic,  convulsive,  33 

degenerative,  542 

de  pensee,  541 

douloureux,  161 

endemic,  541 

general,  541 

generalized,  542 

habit,  541 

hysterical,  542 

local,  541 

mental,  541 

mimic,  107 

psychic,  541 

psychogenous,  542 

spasmodic,  541 
Tinnitus  aurium,  173 

cerebri,  173 
Tongue,  cord  centres  for  muscles  of  the, 
607 

hemiatrophy  of  the,  125 

paralysis  of  the,  124 

spasms  of  the,  124 
Topography,  cranio-cerebral,  600 
Torticollis,  119,  128 
Tortipelvis,  545 
Toxic  factors  in  the  etiology  of  nervous 

diseases,  26 
Tracts  of  the  spinal  cord,  204 
Trance,  596 

hysterical,  503 
Transferred  pains,  diagram  of  location  of, 

147 
Trauma,  as  a  factor  in  the  etiology  of 

nervous  diseases,  25 
Traumatic  hysteria,  533 

neuroses,  533 

psychoses,  533 
Treatment  of  nervous  diseases,  60 
Tremor,  32 

coarse,  32 

fibrillary,  32 

fine,  32 

functional,  44 

hysterical,  501 

intention,  32,  44 

of  paralysis  agitans,  570 

passive,  32 

segmental,  44 


632 


INDEX 


Tremor,  testing  for,  44 

Trigeminus  nerve,  anatomy  of  the,  159 

motor  neuroses  of  the,  106 

sensory  neuroses  of  the,  160 
Trismus,  106 
Trochlear  nerve,  anatomy  of  the,  95 

paralj'sis  of  the,  102 
Trophic  disorders,  576 
Trophoneuroses,  37 

definition  of,  37 

peripheral,  197 
Trousseau's  symptom,  549 
Tubercula  dolorosa,  92 
Tuberculosis,  of  the  brain,  467 
Tuberculous  meningitis,  386 
Tumors,  cerebral,  454 

local  symptoms  of,  458 

of  nerves,  90 

spinal,  318,  320 

vertebro-spinal,  319 
'Tween  brain,  336 
Typewriters'  cramp,  560 

Ulnar  nerve,  paralysis  of  the,  140 
Upper  extremity,  cord  centres  for  muscles 
of  the,  608 

Vagotonia,  117 

Vagus  nerve,  anatomy  of  the,  116 

diseases  of,  117 
Vasomotor  disorders,  576 

neuroses,  peripheral,  197 
Veins,  cerebral,  356 
Vertigo,  174 

arteriosclerotic,  177 

auditory,  176 

Barany's  test  for,  175 

bilious,  176 

essential,  175 

laryngeal,  178 

mechanical,  177 

neuropathic,  176 


Vertigo,  objective,  175 

ocular,  177 

paralyzing,  178 

psychical,  177 

senile,  177 

stomachal,  176 

subjective,  175 
Vestibular  ataxia,  56 

neuroses,  174 
Vibration  sense,  testing  of,  55 
Violinists'  cramp,  564 
Vision,  centres  for,  361 

double,  99 

hj^sterical  disturbances  of,  496 
Volt,  definition  of,  65 
von  Graefe's  symptom,  556 

Waking  numbness,  146 

Wallerian  degeneration,  76 

Watchmakers'  cramp,  564 

Water,  use  of,  in  the  treatment  of  nervous 

diseases,  62 
Watt,  definition  of,  65 
Weber's  syndrome,  443 
Wernicke's  hemiopic  pupillary  reaction, 

158 
Wet  brain,  390 

Whitlow,  analgesic  paraysis  with,  141 
Winking  spasm,  110 
Word  blindness,  368 

deafness,  368,  369 
Work    as    a    factor    in    the    etiology    of 

nervous  diseases,  24 
Wrist-drop,  138 
Writers'  cramp,  560 

treatment,  565 
Wry-neck,  119 

treatment,  119,  122 

X-ray  tests,  57,  70 
Zoophilia,  509 


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